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1
SMITH, JAMES L. "Arthritis and Foodborne Bacteria." Journal of Food Protection 57, no. 10 (October 1, 1994): 935–41. http://dx.doi.org/10.4315/0362-028x-57.10.935.
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Diarrheic episodes caused by the foodborne pathogens Campylobacter, Salmonella, Shigella or Yersinia may lead to a sterile arthritis such as reactive arthritis, Reiter's syndrome or ankylosing spondylitis. Reiter's syndrome and reactive arthritis have been shown to be sequelae in a few well-studied bacterial food poisoning outbreaks. Reactive arthritis, Reiter's syndrome and ankylosing spondylitis show strong familial association related to the gene for HLA-B27 (HLA = human leucocyte antigen) antigen. Why HLA-B27-positive individuals are more susceptible to arthritis is not known, but molecular mimicry between the HLA-B27 antigen and antigens of triggering bacteria has been demonstrated and this mimicry has been proposed as a mechanism involved in etiology of the arthritides. Antigens from bacteria that triggered the arthritis are present in arthritic joints but bacterial cells are not found. Antibodies and T-cells specific for the triggering bacteria have been demonstrated in arthritic patients. T-cells present in synovial joints respond specifically to the particular arthritic triggering pathogen. The cells that respond to bacterial antigens belong to the T-cell subset TH1 that secrete a limited number of cytokines but it is not known if cytokines are involved in arthritis. A few studies have demonstrated that T-cells from the joints of arthritic patients respond to both bacterial and human heat shock proteins indicating that autoimmunity may be involved in causation of arthritis. While only about 2% of a population exposed to a triggering infection will acquire arthritis, these individuals undergo pain and suffering as well as economic hardships as a result of their disease.
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ODEWUSI, OO, MJ ABDULMUMIN, and OO OLANIYAN. "AN ASSESSMENT OF AUTOIMMUNITY IN ARTHRITIS PATIENTS." International Journal of Medical Laboratory Research 07, no. 01 (2022): 53–61. http://dx.doi.org/10.35503/ijmlr.2022.7108.
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Objectives: The goal of this study is to estimate autoimmune biomarkers that characterize the development and severity of arthritis, but probably normalize following successful therapy. Materials and methods: In this study a total of 109 subjects were used out of which treated and untreated arthritics were 48 and 44 respectively, the remaining 17 were healthy individuals which were used as control. Samples were collected from patients attending Rheumatology and Orthopedic clinic of Federal Teaching Hospital Ido-ekiti, Ekiti State Nigeria. Antinuclear antibody was estimated using Enzyme Linked Immunosorbent Assay (ELISA) while Lupus Erythematosus cells were ascertained microscopically using Leishman staining technique. All parameters were assessed in treated and untreated arthritic patients relative to healthy subjects. Body mass index was also calculated. Statistical analysis was done using SPSS. Results: Body mass index and Antinuclear antibodies were significantly higher in treated and untreated arthritics compared to control (P<0.05). When treated and untreated arthritics were compared, Body mass index and Antinuclear antibody were found to be significantly higher in untreated arthritics (P<0.05). Antinuclear antibody and Age correlated directly in untreated arthritics. Lupus Erythematosus cell prevalence was found to be higher in untreated arthritics having a percentage Lupus Erythematosus test positivity of 6.8% compared to the 2.1% seen in treated arthritics. Conclusion: It was found that Autoimmunity in arthritics can be significantly lowered through treatment with Arthritic drugs, diets, life style modifications over a period of time. The study suggests that Antinuclear antibody and Lupus Erythematosus estimations could be adopted as markers of diagnosis, prognosis and monitoring of arthritis.
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Castillero, Estíbaliz, María Paz Nieto-Bona, Carmen Fernández-Galaz, Ana Isabel Martín, María López-Menduiña, Miriam Granado, María Angeles Villanúa, and Asunción López-Calderón. "Fenofibrate, a PPARα agonist, decreases atrogenes and myostatin expression and improves arthritis-induced skeletal muscle atrophy." American Journal of Physiology-Endocrinology and Metabolism 300, no. 5 (May 2011): E790—E799. http://dx.doi.org/10.1152/ajpendo.00590.2010.
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Arthritis is a chronic inflammatory illness that induces cachexia, which has a direct impact on morbidity and mortality. Fenofibrate, a selective PPARα activator prescribed to treat human dyslipidemia, has been reported to decrease inflammation in rheumatoid arthritis patients. The aim of this study was to elucidate whether fenofibrate is able to ameliorate skeletal muscle wasting in adjuvant-induced arthritis, an experimental model of rheumatoid arthritis. On day 4 after adjuvant injection, control and arthritic rats were treated with 300 mg/kg fenofibrate until day 15, when all rats were euthanized. Fenofibrate decreased external signs of arthritis and liver TNFα and blocked arthritis-induced decreased in PPARα expression in the gastrocnemius muscle. Arthritis decreased gastrocnemius weight, which results from a decrease in cross-section area and myofiber size, whereas fenofibrate administration to arthritic rats attenuated the decrease in both gastrocnemius weight and fast myofiber size. Fenofibrate treatment prevented arthritis-induced increase in atrogin-1 and MuRF1 expression in the gastrocnemius. Neither arthritis nor fenofibrate administration modify Akt-FoxO3 signaling. Myostatin expression was not modified by arthritis, but fenofibrate decreased myostatin expression in the gastrocnemius of arthritic rats. Arthritis increased muscle expression of MyoD, PCNA, and myogenin in the rats treated with vehicle but not in those treated with fenofibrate. The results indicate that, in experimental arthritis, fenofibrate decreases skeletal muscle atrophy through inhibition of the ubiquitin-proteasome system and myostatin.
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Baillet, Athan, Candice Trocmé, Xavier Romand, Chuong M. V. Nguyen, Anais Courtier, Bertrand Toussaint, Philippe Gaudin, and Olivier Epaulard. "Calprotectin discriminates septic arthritis from pseudogout and rheumatoid arthritis." Rheumatology 58, no. 9 (March 28, 2019): 1644–48. http://dx.doi.org/10.1093/rheumatology/kez098.
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Abstract Objective We aimed to determine whether calprotectin and α-defensins could discriminate septic from other inflammatory arthritides. Methods Synovial fluids with a predominance of neutrophils from patients with septic arthritis, pseudogout and RA were prospectively collected. Neutrophil-related proteins calprotectin and human neutrophil α-defensins levels were assessed in synovial fluids. Demographic parameters and biomarkers with P-value ⩽0.05 for differentiating septic from non-septic arthritis were included in a multivariable model. Multivariable logistic regression with stepwise selection was performed to build the final combined model. Results A total of 74 patients were included: septic arthritis (n = 26), pseudogout (n = 28) and RA (n = 20). Patients with septic arthritis were more likely to be male and young, and to display higher synovial neutrophil count. Calprotectin was significantly increased in patients with septic arthritis. The multivariable model included calprotectin, synovial fluid neutrophil count and gender. Calprotectin was the only biomarker that discriminated septic arthritis from non-septic inflammatory arthritides, with 76% sensitivity, 94% specificity and a positive likelihood ratio = 12.2 at the threshold for calprotectin of 150 mg/l. Conclusion Synovial fluid calprotectin is a relevant biomarker to discriminate septic arthritis from other inflammatory arthritides. This biomarker should be tested in an independent cohort.
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Gómez-SanMiguel, Ana Belén, Ana Isabel Martín, Maria Paz Nieto-Bona, Carmen Fernández-Galaz, María López-Menduiña, María Ángeles Villanúa, and Asunción López-Calderón. "Systemic α-melanocyte-stimulating hormone administration decreases arthritis-induced anorexia and muscle wasting." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 304, no. 10 (May 15, 2013): R877—R886. http://dx.doi.org/10.1152/ajpregu.00447.2012.
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Rheumatoid cachexia is associated with rheumatoid arthritis and it increases mortality and morbidity. Adjuvant-induced arthritis is an experimental model of rheumatoid arthritis that causes anorexia and muscle wasting. α-Melanocyte-stimulating hormone (α-MSH) has anti-inflammatory actions, and it is able to decrease inflammation in several inflammatory diseases including experimental arthritis. In this study we tested whether systemic α-MSH treatment is able to ameliorate cachexia in arthritic rats. On day 8 after adjuvant injection control and arthritic rats were treated with α-MSH (50 μg/rat ip) twice a day, until day 16 when all rats were euthanized. Arthritis decreased food intake, but it increased hypothalamic expression of neuropeptide Y (NPY) and Agouti-related peptides (AgRP) as well as interleukin-1β (IL-1β) and cyclooxygenase-2 (COX-2) mRNA. In arthritic rats, α-MSH decreased the external signs of arthritis and increased food intake ( P < 0.01). In addition, α-MSH decreased hypothalamic expression of IL-1β, COX-2, proopiomelanocortin, and prohormone-converting (PC) enzymes PC1/3 and PC2 mRNA in arthritic rats. In control rats, α-MSH did not modify food intake or hypothalamic expression of aforementioned mRNA. α-MSH prevented arthritis-induced increase in gastrocnemius COX-2, muscle-specific RING-finger protein-1 (MuRF1), and atrogin-1 expression, and it increased fast myofiber size. In conclusion our data show that in arthritic rats peripheral α-MSH treatment has an anti-cachectic action increasing food intake and decreasing muscle wasting.
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Dalix, E., M. Maalouf, A. Vanden-Bossche, M. Paul, and H. Marotte. "OP0208 MECHANICAL UNLOADING PREVENTED ARTHRITIS IN THE RAT ADJUVANT-INDUCED ARTHRITIS MODEL." Annals of the Rheumatic Diseases 82, Suppl 1 (May 30, 2023): 137.1–137. http://dx.doi.org/10.1136/annrheumdis-2023-eular.3762.
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BackgroundRheumatoid arthritis (RA) is the most common chronic inflammatory rheumatic disease, characterized by synovitis associated with progressive bone loss and joint swelling. The adjuvant-induced arthritis (AIA) model mimics the pathophysiological features of RA, with a very high prevalence and reproducibility. YAP plays a key role in synovial hyperplasia. It is a transcription factor which can be activated in response to inflammation but also by a mechanical stimulus as tissue stiffening. We already showed a decrease arthritis severity by inhibiting YAP in the AIA model [1]. Then, different mechanical challenges could potentially impact arthritis development by regulating YAP.ObjectivesThe objective of this study was to investigate the impact of mechanical loading and unloading on the development of arthritis in the AIA model.MethodsArthritis was induced in female Lewis rats by injection of the adjuvantMycobacterium butyricum, defining day (D)0. The AIA model normally develops arthritis at D10, with a peak of inflammation at D17 [2]. Rats were randomized into three groups: an AIA+mechanical loading group (n=11) with free access to an activity wheel from D0 to D17, an AIA+mechanical unloading group (n=11) by tail suspension from D0 to D17, and an AIA-only group (n=11) as positive control. Daily clinical monitoring (arthritic index and ankle circumference) was used to follow the progression and severity of arthritis. At D17, the ankles of the rats were collected to perform RT-qPCR.ResultsArthritis onset was observed at the same time (D10) in the AIA control and AIA+mechanical loading groups with the same kinetic of arthritis index and ankle circumferences. However, the majority of rats in the AIA+mechanical unloading group did not develop any signs of arthritis. At D17, gene expression of YAP and CYR61 (YAP target gene), IL1B, IL6, RANKL, ACP5 (encoding TRAPc), CTSK (encoding cathepsin K), MMP9, and MMP13 was decreased in the ankle of AIA+mechanical unloading rats compared to other groups. In the AIA+ mechanical loading group, rat stopped their physical activity at D10 which may explain the lack of clinical and molecular differences between the AIA and AIA+mechanical loading groups at D17.Figure 1.Arthritic index from day(D) 0 to D17 in the AIA control (CTR) group (n=11), the AIA+mechanical loading (WHEEL) group (n=11) and the AIA+mechanical unloading (SUSP) group (n=11).ConclusionMechanical unloading of the hindpaws by the suspension system strongly prevented arthritis by a reduced expression of pro-inflammatory genes, bone resorption, and bone degradation genes. The decrease in inflammation may be partly explained by the decrease in YAP transcriptional activity. Mechanical stress is therefore a key factor in inflammation during AIA. The precise mechanisms linking these two mechanisms are still under investigation.References[1]Caire R, Audoux E, Courbon G, Michaud E, Petit C, Dalix E, et al. YAP/TAZ: Key Players for Rheumatoid Arthritis Severity by Driving Fibroblast Like Synoviocytes Phenotype and Fibro-Inflammatory Response.Front Immunol2021;12:791907.[2]Courbon G, Cleret D, Linossier M-T, Vico L, Marotte H. Early Subchondral Bone Loss at Arthritis Onset Predicted Late Arthritis Severity in a Rat Arthritis Model: EARLY BONE LOSS AT ARTHRITIS.J Cell Physiol2017;232:1318–1325. Available at:http://doi.wiley.com/10.1002/jcp.25601. Accessed October 20, 2020.Acknowledgements:NIL.Disclosure of InterestsNone Declared.
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Gómez-SanMiguel, Ana Belén, Carolina Gomez-Moreira, María Paz Nieto-Bona, Carmen Fernández-Galaz, Maria Ángeles Villanúa, Ana Isabel Martín, and Asunción López-Calderón. "Formoterol decreases muscle wasting as well as inflammation in the rat model of rheumatoid arthritis." American Journal of Physiology-Endocrinology and Metabolism 310, no. 11 (June 1, 2016): E925—E937. http://dx.doi.org/10.1152/ajpendo.00503.2015.
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Adjuvant-induced arthritis is an experimental model of rheumatoid arthritis that is associated with body weight loss and muscle wasting. β2-adrenergic receptor agonists are powerful anabolic agents that trigger skeletal muscle hypertrophy and have been proposed as a promising treatment for muscle wasting in human patients. The aim of this work was to determine whether formoterol, a selective β2-adrenoreceptor agonist, is able to ameliorate muscle wasting in arthritic rats. Arthritis was induced in male Wistar rats by intradermal injection of Freund's adjuvant. Control and arthritic rats were injected daily with 50 μg/kg sc formoterol or saline for 12 days. Body weight change, food intake, and arthritis index were analyzed. After euthanasia, in the gastrocnemius mRNA was analyzed by PCR, and proteins were analyzed by Western blotting. Arthritis decreased gastrocnemius weight, cross-sectional area, and myofiber size, whereas formoterol increased those variables in both arthritic and control rats. Formoterol decreased the external signs of arthritis as well as NF-κB(p65) activation, TNFα, and COX-2 levels in the gastrocnemius of arthritic and control rats. Those effects of formoterol were associated with a decreased expression of myostatin, atrogin-1, and MuRF1 and in LC3b lipidation. Arthritis increased the expression of MyoD, myogenin, IGF-I, and IGFBP-3 and -5 in the gastrocnemius. In control and in arthritic rats, treatment with formoterol increased Akt phosphorylation and myogenin levels, whereas it decreased IGFBP-3 expression in the gastrocnemius. These data suggest that formoterol has an anti-inflammatory effect and decreases muscle wasting in arthritic rats through increasing Akt activity and myogenin and decreasing myostatin, the p-NF-κB(p65)/TNF pathway, and IGFBP-3.
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Jacobs, C., D. Young, S. Tyler, G. Callis, S. Gillis, and P. J. Conlon. "In vivo treatment with IL-1 reduces the severity and duration of antigen-induced arthritis in rats." Journal of Immunology 141, no. 9 (November 1, 1988): 2967–74. http://dx.doi.org/10.4049/jimmunol.141.9.2967.
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Abstract IL-1 has been implicated in the pathogenesis of arthritis. Although IL-1 injected in vivo into normal joints results in a transient inflammatory reaction, we have shown that three weekly repetitive injections of IL-1 do not produce a progressive inflammatory condition suggestive of chronic arthritis. In fact, priming normal joints with three weekly IL-1 intraarticular injections results in a significant reduction in joint swelling and diminished histopathologic alterations/lesions caused by subsequent methylated BSA-induced arthritis. Similarly, post treatment with IL-1 intraarticular injection after arthritis induction reduced arthritic swelling and joint injury if IL-1 was given during the developing stage of arthritis. Our results suggest that IL-1 might limit arthritic inflammation and progressive cartilage destruction through an, as yet, undetermined mechanism(s). Further in vivo investigations are required to determine the therapeutic utility of IL-1 in reducing early arthritic inflammation.
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Zhang, Kevin, June Liu, Jilin Deng, Liangtang Chang, Jian Shao, Jun Lu, Alison Bendele, Yunfeng Fu, and Jeff Duan. "Modeling human rheumatoid arthritis in NHP: Type II collagen induced arthritis in cynomolgus macaques (167.4)." Journal of Immunology 186, no. 1_Supplement (April 1, 2011): 167.4. http://dx.doi.org/10.4049/jimmunol.186.supp.167.4.
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Abstract Collagen induced arthritis (CIA) rodent models have been extensively used in rheumatoid arthritis (RA) research. An RA model in non-human primate (NHP) is particularly demanded because of the close phylogenesis that provides the cross-reactivity to human for different development compounds using most modern drug technologies. However, NHP RA model has been reported extremely difficult because of the low and inconsistent disease incidence. We studied type II collagen induced arthritis in Cynomolgus monkeys. Following immunization with collagen, the disease progression was monitored for 8 weeks. Overall the arthritic incidence reached 87% and the average arthritic incidence of proximal interphalangeal (PIP) joint reached near 90%, significantly higher than what was previously reported. The average swelling of PIP joint increased approximately by 45%. Radiography, histopathology and histomorphometry analysis of the joint bones well supported the arthritic disease with the similar characteristics of human RA joints. The average arthritic score was significantly reduced with the single agent treatment of Methotrexate or Dexamethasone. Our results demonstrated the successful establishment of an reliable CIA in Cynomolgus monkeys, providing a valuable tool for studies of RA disease in pathogenesis, biomarker, translational research, and most importantly, anti-arthritic therapeutics as well as other relevant diseases, such as anemia of chronic disease and arthritic pain.
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Faustino, Célia, Noélia Duarte, and Lídia Pinheiro. "Triterpenes Drug Delivery Systems, a Modern Approach for Arthritis Targeted Therapy." Pharmaceuticals 17, no. 1 (December 28, 2023): 54. http://dx.doi.org/10.3390/ph17010054.
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Arthritis is a major cause of disability. Currently available anti-arthritic drugs, such as disease-modifying anti-rheumatic drugs (DMARDs), have serious side-effects associated with long-term use. Triterpenoids are natural products with known anti-inflammatory properties, and many have revealed efficiency against arthritis both in vitro and in vivo in several animal models, with negligible cytotoxicity. However, poor bioavailability due to low water solubility and extensive metabolism upon oral administration hinder the therapeutic use of anti-arthritic triterpenoids. Therefore, drug delivery systems (DDSs) able to improve the pharmacokinetic profile of triterpenoids and achieve sustained drug release are useful alternatives for targeted delivery in arthritis treatment. Several DDSs have been described in the literature for triterpenoid delivery, including microparticulate and nanoparticulate DDSs, such as polymeric micro and nanoparticles (NPs), polymeric micelles, liposomes, micro and nanoemulsions, and hydrogels. These systems have shown superior therapeutic effects in arthritis compared to the free drugs and are similar to currently available anti-arthritic drugs without significant side-effects. This review focuses on nanocarriers for triterpenoid delivery in arthritis therapy, including osteoarthritis (OA), rheumatoid arthritis (RA) and gout that appeared in the literature in the last ten years.
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Castillero, Estíbaliz, María López-Menduiña, Ana Isabel Martín, María Ángeles Villanúa, and Asunción López-Calderón. "Comparison of the effects of the n-3 polyunsaturated fatty acid eicosapentaenoic and fenofibrate on the inhibitory effect of arthritis on IGF1." Journal of Endocrinology 210, no. 3 (June 29, 2011): 361–68. http://dx.doi.org/10.1530/joe-11-0170.
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Adjuvant-induced arthritis is a chronic inflammatory illness that induces muscle wasting and decreases circulating IGF1. Eicosapentaenoic acid (EPA) and fenofibrate, a peroxisome proliferator-activated receptors α agonist, have anti-inflammatory actions and ameliorate muscle wasting in arthritic rats. The aim of this work was to elucidate whether EPA and fenofibrate administration are able to prevent the effect of arthritis on the IGF1–IGFBP system. On day 4 after adjuvant injection control, arthritic rats were gavaged with EPA (1 g/kg) or fenofibrate (300 mg/kg) until day 15 when all rats were killed. Arthritis decreased body weight gain, serum IGF1, and liverIgf1mRNA, whereas it increased gastrocnemiusIgfbp3mRNA. EPA, but not fenofibrate, administration prevented arthritis-induced decrease in serum IGF1 and liverIgf1mRNA. In the rats treated with EPA arthritis increasedIgfbp5mRNA in the gastrocnemius. Fenofibrate treatment decreased IGF1 andIgf1mRNA in the liver and gastrocnemius. In arthritic rats, fenofibrate increased body weight gain and decreased gastrocnemiusIgfbp3andIgfbp5mRNA. These data suggest that the mechanisms through which EPA and fenofibrate act on the IGF1 system and ameliorate muscle wasting in arthritic rats are different. EPA administration increased circulating levels of IGF1, whereas fenofibrate decreased theIgfbp3andIgfbp5in the gastrocnemius muscle.
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Sewell, J., S. M. Hussain, Y. Wang, A. Wluka, M. Carrrington, K. Samaras, and F. Cicuttini. "POS0525 ARTHRITIC PAIN AS A SURROGATE MARKER FOR ASYMPTOMATIC CARDIOVASCULAR RISK FACTORS: OFFERING PRACTITIONERS A ‘TEACHABLE MOMENT’." Annals of the Rheumatic Diseases 80, Suppl 1 (May 19, 2021): 496.1–496. http://dx.doi.org/10.1136/annrheumdis-2021-eular.1763.
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Background:Cardiovascular diseases (CVD) are the number one cause of death worldwide. CVDs are linked to well established risk factors: obesity, hypertension (HTN), dyslipidaemia (DL) and diabetes mellitus (DM)1. While targeting risk factors reduces the burden of CVD, this is often challenging because they are largely asymptomatic and patients are therefore unlikely to seek medical attention. Arthritis, in contrast, causes pain and functional impairment prompting presentation to a healthcare practitioner. Patients with arthritis of varying aetiologies (such as osteoarthritis2, gout3, rheumatoid arthritis4) have been shown to have an increased risk of CVD.Objectives:To examine the relationship between arthritis and DM, HTN and DL in adults of all age groups. A secondary objective was to examine whether this relationship existed independent of obesity.Methods:Data from the 2017-18 Australian Bureau of Statistics National Health Survey included 13,776 participants, categorised into young (18-39 years), middle aged (40-64 years) and older (≥65 years) adults. Blood pressure, height and weight were measured. BMI was calculated and participants classified as obese (≥30 kg/m2) or non-obese. HTN was defined as > 140/90mmHg. Participants were asked if they had arthritis of any form, DL or DM diagnosed by a doctor. Logistic regression models estimated odds ratios with 95% CI for prevalence of arthritis associated with CVD risk factors.Results:Arthritis was reported by 3.9% of young adults, 28.8% of middle-aged adults, and 54.5% ofolderadults. In all three age groups, arthritis was associated with significantly increased odds of obesity, HTN, DL and DM. For example, in middle-aged adults, having arthritis was associated with increased odds of obesity (1.75, 95% CI 1.54-2.01), HTN (1.78, 1.60-2.04), DL (2.14, 1.84-2.49) and DM (1.64, 1.33-2.03). These associations remained statistically significant after adjustment for obesity.Conclusion:Compared to those without arthritis, adults with arthritis were at increased risk of obesity, HTN, DM and DL. The increased risk of HTN, DM and DL was independent of obesity and tended to be higher in younger adults. These data suggest that a patient’s presentation with symptomatic arthritis of any aetiology and at any age, may be used opportunistically as a “teachable moment” for screening for asymptomatic CVD risk factors in higher-risk individuals. This provides practitioners an opportunity to manage both arthritis and CVD risk in parallel, rather than in silos.References:[1]World Health Organisation. (2017). “Cardiovascular Diseases.” from https://www.who.int/en/news-room/fact-sheets/detail/cardiovascular-diseases(cvds).[2]Wang, H., et al. (2016). “Osteoarthritis and the risk of cardiovascular disease: a meta-analysis of observational studies.” Scientific reports 6: 39672.[3]Singh, J. (2015). “When gout goes to the heart: does gout equal a cardiovascular disease risk factor?” Annals of the Rheumatic Diseases 74: 631-634.[4]England, B. R., et al. (2018). “Increased cardiovascular risk in rheumatoid arthritis: mechanisms and implications.” British Medical Journal 361: k1036.Table 1.Prevalence of CVD risk factors in adults with and without arthritis.Young18-39 yoMiddle Aged40-64 yoOlder≥65 yoNo arthritisn = 3773Arthritisn = 157OR (95% CI)*adjusted for obesityNo arthritisn = 4055Arthritisn = 1638OR (95% CI)*adjusted for obesityNo arthritisn = 1891Arthritisn = 2262OR (95% CI)*adjusted for obesityObesity473322.07 (1.36-3.16)8685271.75 (1.54-2.01)3266101.89 (1.62-2.21)HTN131142.72 (1.53-4.84)2.35 (1.17-4.70)*7454961.78 (1.60-2.04)1.59 (1.37-1.84)73010911.48 (1.31-1.68)1.35 (1.18-1.55)*DM1945.7 (1.74-15.37)4.87 (1.34-17.69))*2361511.64 (1.33-2.03)1.37 (1.08-1.73)*2563991.37 (1.15-1.62)1.15 (0.95-1.39)*Disclosure of Interests:None declared
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Mu, Hong-Hua, Shaowei Jiang, Xingqiong Wang, Connor Meaney, and Jingyi Wang. "Synergetic effect of an autoantigen CII and a mycoplasma superantigen on the onset and development of autoimmune arthritis in mice." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 178.9. http://dx.doi.org/10.4049/jimmunol.202.supp.178.9.
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Abstract An infection can amplify an autoimmune disease by either exacerbating an ongoing disorder, including a relapse, or by leading to chronic progressive disease. We have been studying a mouse autoimmune arthritis induced by M. arthriditis. M. arthritidis produces a potent superantigen (SAg) MAM, which is shown to be partially responsible for the chronic autoimmune arthritis. Although the MAM clearly plays a role in disease induced by live M. arthritidis, MAM alone does not induce overt disease. It does alter the immune system rendering mice more susceptible to disease that caused by other autoimmune agents such as type II collagen (CII). A key question however is how do CII and MAM act together in the host to initiate inflammation and then an autoimmune arthritis? MAM was injected into mice convalescing from CIA or mice suboptimally immunized with CII. In contrast to controls, MAM caused an exacerbation of arthritis in mice that were recovering from CIA. MAM also triggered arthritis onset in mice that had been immunized with CII up to 71 days previously. Injection of MAM during the onset phase of CIA also triggered and enhanced the severity of arthritis in mice given low doses of CII. We also tested the CII-specific immune responses in mice injected with CII alone and also to the mixtures of the CII and MAM. The T cell profile analysis demonstrated that MAM significantly promoted IL-17 and IFNg following exposure to CII in vivo. Of particular interest was that MAM-enhanced IL-17 can stimulate synoviocytes to release a spectrum of chemokines, CXCL1, CXCL2, CXCL12, CCL2 and CCL5, and attracted inflammatory leukocytes. Thus, the results suggest MAM can serve as an enhancer and a trigger by activating inflammatory responses to other bioactive molecules, i.e. CII.
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Ezeani, Nkiru N. "Anti-Arthritic and Antioxidant Efficacy of Ethanol and Aqueous Root Extracts of Olax subscorpioidea in CFA-Induced Arthritic Rats." NEWPORT INTERNATIONAL JOURNAL OF RESEARCH IN MEDICAL SCIENCES 5, no. 2 (May 30, 2024): 48–56. http://dx.doi.org/10.59298/nijrms/2024/5.2.04856.
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The traditional use of Olax subscorpioidea root extracts for arthritis management in rural areas, where NSAIDs and biologic drugs are unaffordable, lacks scientific validation. This study aimed to investigate the anti-arthritic and antioxidant properties of ethanol and aqueous root extracts of Olax subscorpioidea Afzel in albino rats with adjuvant-induced arthritis. A total of 135 albino rats were divided into nine groups of 15 rats each. Rheumatoid arthritis (RA) was induced in groups 2-9 through intradermal injection of 0.1 ml Chicken type II collagen-Complete Freund’s adjuvant in the left hind paw. Starting from day 10 post-induction, the rats were treated with the extracts at doses of 400, 600, and 800 mg/kg body weight for 32 days. Sample analysis was conducted using spectrophotometric methods. Arthritic rats exhibited significantly elevated levels of nitric oxide (NO) and malondialdehyde (MDA) (P<0.05) and reduced levels of superoxide dismutase (SOD), catalase, glutathione peroxidase, reduced glutathione, and tocopherol compared to normal control rats. Treatment with Olax subscorpioidea extracts significantly reversed these effects in a time- and dose dependent manner. The efficacy of the extracts was comparable to the standard drug indomethacin (P<0.05). This study provides scientific evidence that ethanol and aqueous root extracts of Olax subscorpioidea possess significant anti-arthritic and antioxidant activities. These extracts potentially enhance antioxidant levels, reduce oxidative stress, and mitigate arthritic conditions, supporting their traditional use and suggesting potential therapeutic applications in rheumatoid arthritis management. Keywords: Anti-arthritic, Antioxidant, Olax subscorpioidea, Rheumatoid Arthritis, Oxidative Stress, Ethanol Extract, Aqueous Extract, Adjuvant-Induced Arthritis
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MA, Dar. "Anti-Arthritic Activity of Leaf of Carissa carandas (L) against Adjuvant- Induced Arthritis in Rat." Journal of Natural & Ayurvedic Medicine 3, no. 2 (April 16, 2019): 1–8. http://dx.doi.org/10.23880/jonam-16000187.
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Background: Carissa carandas (Apocynaceae) also known as Karonda. The plant has been used in Ayurveda, Unani and Homoeopathic system medicine for over thousands of years. The leaves of this plant has shown astringent, antidiabetic, anti-inflammation and anti-pyretic activity and also used in the rheumatism. Objectives: The present investigation was carried out to evaluate the anti-arthritic activity of ethanolic extract of leaf of Carissa carandas against adjuvant - induced arthritis in rat. Materials and Methods: In this study both male as well as female Wister arts were used in the study. Arthritis was induced by injecting 0.1ml of freund’s complete adjuvant intra-dermally into the left hind paw of the rats. The paw volume, hematological, biochemical, radiographic and histopathological study were evaluated. Results: The extract shows significant reduction in the paw volume which was comparable with the standard and treated as well as normal group. The study reveals that extract as well as standard group shows mild reduction of paw volume where as in negative control sclerosis was seen. The changes in haematological parameters adjuvant induced arthritis shown there was significant increase of RBC count and haemoglobin, while there was significant decrease in WBC count and ESR of arthritic rats in comparison to control. The biochemical parameters such as ALT, ALP, and AST in arthritis induced by CFA group 2 it also showed that the administration of Carissa carandas at doses of 200mg and 400mg/kg in group 4, 5 and standard, in which a significant difference in the triglycerides was found. Conclusion: The effect of anti-arthritic activity of ethanolic extract of leaf of Carissa carandas was investigated in the present study may be due to synergistic effect of phytoconstituents, since the plant contains the active principle which are able to target through multiple mechanisms and which is used in pathophysiology of arthritis.
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Wang, Yanming, Tao He, Zhiming Li, and Shujun Gai. "Effect of ethanol extract of Punica granatum L against Freund’s complete adjuvant-induced arthritis in rats." Tropical Journal of Pharmaceutical Research 18, no. 3 (May 14, 2021): 591–95. http://dx.doi.org/10.4314/tjpr.v18i3.21.
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Purpose: To investigate the protective effect of ethanol extract of P. granatum against arthritis in rat model.
Methods: Twenty-six adult male Wistar rats (120 - 150 g) were separated into four groups (n = 6): normal control, arthritic control and two treatment groups. With the exception of normal control group, arthritis was induced by intraplantar administration of Freund’s complete adjuvant (FCA) on the 1st day of drug administration. The arthritic control group was not treated, while the treatment groups received extract orally at 500 or 750 mg/kg for the period of 4 weeks and at the end of each week, paw volume, thermal hyperalgesia, arthritic score and mechanical nociceptive threshold were performed to assess arthritis. Biochemical indicators and inflammatory cytokines in serum were determined using standard procedures.
Results: There was significant decrease in paw volume and arthritic score; paw withdrawal latency was enhanced in extract-treated groups, compared to arthritic control group (p < 0.05). Furthermore, ALT, AST and ALP levels, as well as RF and MDA activities decreased significantly with extract treatment, compared with arthritic control group (p < 0.05). Treatment with the extract attenuated the altered level of interleukin 1β (IL-1β) and TNF-α levels in arthritic rats. Histological examination showed that treatment with the extract significantly reversed histological changes induced by arthritis.
Conclusion: The results reveal that the beneficial effect of ethanol extract of P. granatum against FCAinduced arthritis is due to its ability to reduce the levels of inflammatory cytokines.
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López-Menduiña, María, Ana Isabel Martín, Estíbaliz Castillero, María Angeles Villanúa, and Asunción López-Calderón. "Systemic IGF-I administration attenuates the inhibitory effect of chronic arthritis on gastrocnemius mass and decreases atrogin-1 and IGFBP-3." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 299, no. 2 (August 2010): R541—R551. http://dx.doi.org/10.1152/ajpregu.00211.2010.
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Adjuvant arthritis is an animal model of rheumatoid arthritis that decreases liver and circulating IGF-I as well as skeletal muscle mass. The aim of this work was to elucidate whether IGF-I administration was able to prevent the effect of arthritis on body weight and on two skeletal muscles, gastrocnemius and soleus. On day 4 after adjuvant injection, control and arthritic rats were treated with IGF-I (100 μg/kg sc) two times a day, until day 15 when all rats were killed. Arthritis decreased body weight gain and gastrocnemius weight. In arthritic rats, IGF-I treatment increased body weight gain and gastrocnemius weight, without modifying food intake or the external signs of arthritis. Arthritis increased atrogin-1 and muscle ring finger 1 (MuRF1) gene expression in the gastrocnemius and to a lesser extent in the soleus muscle. IGF-I attenuated the arthritis-induced increase in atrogin-1 and MuRF1 expression in the gastrocnemius, whereas it did not modify the expression of these genes in the soleus muscle. Arthritis also increased IGF-binding protein (IGBP)-3 and IGFBP-5 gene expression in gastrocnemius and soleus, whereas IGF-I administration decreased IGFBP-3, but not IGFBP-5, gene expression in both muscles. In both groups of arthritic rats and in control rats treated with IGF-I, proliferating cell nuclear antigen and myogenic differentiation proteins were increased in the gastrocnemius. These data suggest that the inhibitory effect of chronic arthritis on skeletal muscle is higher in fast glycolytic than in slow oxidative muscle and that IGF-I administration attenuates this effect and decreases atrogin-1 and IGFBP-3 gene expression.
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Johnson, Sheena, David Sidebottom, Felix Bruckner, and David Collins. "Identification of Mycoplasma fermentans in Synovial Fluid Samples from Arthritis Patients with Inflammatory Disease." Journal of Clinical Microbiology 38, no. 1 (January 2000): 90–93. http://dx.doi.org/10.1128/jcm.38.1.90-93.2000.
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ABSTRACT Since 1970 Mycoplasma fermentans has been suspected of being associated with rheumatoid arthritis. However, this association has been difficult to prove, and this has been our goal. The distribution of M. fermentans was studied in the synovial fluid of patients suffering from different arthritides. Samples of synovial fluid were taken from patients with well-defined disease and a clear diagnosis. After removal of the inflammatory cells and hyaluran, they were treated with proteinase K and tested by a single or fully nested PCR with primers directed against part of the two 16S rRNA genes of M. fermentans . The product was sequenced automatically, by using an ALF Express automatic sequencer, to confirm the mycoplasma species and to identify the strain since the two genes were usually found to be polymorphic. This was also true of the type strain, strain PG18. M. fermentans was detected in 23 of 26 (88%) rheumatoid arthritis patients, and four different strains were found. It was also found in 7 of 8 (88%) of the nonrheumatoid inflammatory arthritis patient group, which consisted of one patient with reactive arthritis, one patient with pauciarticular juvenile chronic arthritis, two patients with gout, two patients with ankylosing spondylitis, and two patients with psoriatic arthritis, only one of whom was infected with M. fermentans . It was not detected in any of the 10 osteoarthritis patients. M. fermentans was therefore found to be a variable and very common organism in arthritic patients with inflammatory joint exudates and may well prove to be important in the etiology of the diseases.
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Shih, Lih-Yuann, Jiunn-Jer Wu, and Wai-Hee Lo. "Changes in Gait and Maximum Ankle Torque in Patients with Ankle Arthritis." Foot & Ankle 14, no. 2 (February 1993): 97–103. http://dx.doi.org/10.1177/107110079301400208.
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Findings from quantitative gait analysis and maximum ankle torque were used to assess the walking pattern of patients with ankle arthritis and to correlate the changes of gait parameters and muscle strength with severity of arthritis. Gait analysis and the isokinetic maximum ankle torque test were performed in 20 patients with first to fourth degree traumatic ankle arthritis. Six patients without evidence of traumatic arthritis were used as controls. Isokinetic maximum ankle plantarflexion and dorsiflexion torques were determined with Cybex instrumentation. Force plate and foot switch data were gathered during level walking. Maximum ankle plantarflexion and dorsi flexion torques were diminished in the injured ankles. Velocity, stride length, and cadence were decreased in arthritic patients compared with controls. The arthritic limbs had shorter single limb stance and longer double stance during free and fast walking speeds compared with the controls’ affected ankles. The patterns of ground reaction forces were similar in the injured and uninvolved limbs as well as the control subjects, except the magni tude of vertical forces during push-off were reduced in arthritic ankles. The gait parameters and muscle strength deteriorated as the arthritis became severe, but they showed significant changes only when the patients had third or fourth degree arthritis.
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Holland, Sara, James Dickey, Louis Ferreira, and Emily Lalone. "Investigating the grip forces exerted by individuals with and without hand arthritis while swinging a golf club with the use of a new wearable sensor technology." Proceedings of the Institution of Mechanical Engineers, Part P: Journal of Sports Engineering and Technology 234, no. 3 (June 16, 2020): 205–16. http://dx.doi.org/10.1177/1754337120923838.
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Hand arthritis is the leading cause of disability in individuals over the age of 50, causing impairments in grip strength and range of motion. Golf is often recommended to patients with hand arthritis as a low-impact sport to maintain a healthy lifestyle. As such, numerous “arthritic” golf grips have been marketed, but lack quantitative measures to justify their use. The objective of this study was to quantify the differences in total applied grip force in golfers with/without hand arthritis using several types of golf grips. Twenty-seven participants (17 without and 10 with hand arthritis) were evaluated swinging mid-iron clubs with 12 different golf grip designs (9 standard and 3 “arthritic”). The trail hand thumb, index, middle, and ring finger applied grip forces were measured using the wireless FingerTPS system. Finger grip configuration (finger joint angles) of the thumb and index were measured using the Dartfish Movement Analysis Software paired with the newly developed Grip Configuration Model to obtain grip range of motion. Results indicated that golfers with hand arthritis had a significant deficit of 45% golf grip strength (P = 0.02). In addition, individuals with hand arthritis exhibited larger forces in 11 out of 12 golf grips tested when compared with their maximum golf grip strength. Despite how these grips are marketed, there are no “savings” in finger force or grip configuration when using the “arthritic” designed golf grips. Therefore, these grips may not be beneficial for patients with hand arthritis.
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Puri, Kamal D., Bart H. Steiner, Adam S. Kashishian, Hao Chen, W. Michael Gallatin, and Neill A. Giese. "IC87114, a Selective Inhibitor of PI3Kδ Suppresses Joint Inflammation and Bone Erosion in Collagen-Induced Arthritis in Rat (50.14)." Journal of Immunology 182, no. 1_Supplement (April 1, 2009): 50.14. http://dx.doi.org/10.4049/jimmunol.182.supp.50.14.
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Abstract PI3Kδ plays an essential role in antigen-receptor signaling, proliferation, activation and function of lymphocytes. Mice deficient in PI3Kδ activity show substantial reduction in immunoglobulin levels, partial impairment in chemoattractant-induced neutrophil migration as well as defects in signaling and function of macrophages. Collagen-induced arthritis (CIA), a commonly used model for studying antirheumatic drugs, requires participation of both B and T cells to initiate disease and reproduces many of the pathogenic mechanisms detected in human rheumatoid arthritis. In this study, we have investigated the ability of IC87114, a selective PI3Kδ inhibitor, to reverse the rheumatoid arthritic like state in the CIA model of arthritis. Clinical arthritis was initiated by immunizing animals with collagen followed by a booster dose on day 7. IC87114 or control treatment was initiated when at least one hind paw was significantly inflamed and continued for an 18-day treatment course. IC87114-treatment of arthritic rats reduced the progression and severity of clinical arthritis that was evident within 6 days after initiation of therapy. IC87114-treatment significantly reduced the level of anti-collagen antibodies. Arthritic rats treated with IC87114 had significantly lower radiographic scores compared with control, indicating that treatment with IC87114 was effective in protecting bone integrity. Histopathological evaluation demonstrated that IC87114 was effective in reducing the histological changes induced by rheumatoid arthritis. The effect of IC87114-treatment on these parameters together suggests a therapeutic potential for PI3Kδ-selective compounds to ameliorate rheumatoid arthritis.
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Honke, Nadine, Clemens J. Wiest, and Georg Pongratz. "β2-Adrenergic Receptor Expression and Intracellular Signaling in B Cells Are Highly Dynamic during Collagen-Induced Arthritis." Biomedicines 10, no. 8 (August 11, 2022): 1950. http://dx.doi.org/10.3390/biomedicines10081950.
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The sympathetic nervous system (SNS) has either a pro-inflammatory or anti-inflammatory effect, depending on the stage of arthritis. In the past, treatment of arthritic B cells with a β2-adrenergic receptor (β2-ADR) agonist has been shown to attenuate arthritis. In this study, the expression and signaling of β2-ADR in B cells during collagen-induced arthritis (CIA) were investigated to provide an explanation of why only B cells from arthritic mice are able to improve CIA. Splenic B cells were isolated via magnetic-activated cell sorting (MACS). Adrenergic receptors on B cells and intracellular β2-ADR downstream molecules (G protein-coupled receptor kinase 2 (GRK-2), β-Arrestin 2, p38 MAPK, extracellular signal-regulated kinase 1/2 (ERK1/2) and cAMP response element-binding protein (CREB)) were analyzed at different time points in naïve and arthritic B cells with and without stimulation of β2-ADR agonist terbutaline by flow cytometry. β2-ADR-expressing B cells increase during CIA without a change in receptor density. Moreover, we observed a profound downregulation of GRK-2 shortly after induction of arthritis and an increase in β-Arrestin 2 only at late stage of arthritis. The second messengers studied (p38, ERK1/2 and CREB) followed a biphasic course, characterized by a reduction at onset and an increase in established arthritis. Stimulation of CIA B cells with the β-ADR agonist terbutaline increased pp38 MAPK independent of the timepoint, while pERK1/2 and pCREB were enhanced only in the late phase of arthritis. The phosphorylation of p38 MAPK, ERK1/2 and CREB in the late phase of arthritis was associated with increased IL-10 produced by B10 cells. The change of β2-ADR expression and signaling during sustained inflammation might be an integral part of the switch from pro- to anti-inflammatory action of sympathetic mechanisms in late arthritis.
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Neeraj, Srivastava, Dashora Nipun, Menaria Jyoti, and Kumar Neeraj. "Evaluation of Anti-inflammatory and Anti-arthritic Activity of Ajmodadi Churna- A Polyherbal Formulation." International Journal of Pharmaceutical and Phytopharmacological Research 6, no. 5 (October 30, 2016): 72. http://dx.doi.org/10.24896/eijppr.2016651.
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Anti-inflammatory and anti- arthritic activity of aqueous extract of Ajmodadi Churna (AJM) were evaluated by three methods namely, Carrageenan paw edema, Carrageenan induced Air Pouch Model in Rats and Freunds’ complete adjuvant Arthritis. The Carrageenan paw edema was carried out to test the effect of the extract on acute phase of inflammation. Carrageenan induced Air Pouch Model was used for local inflammation and Freunds’ complete adjuvant Arthritis was used for evaluation of chronic inflammation. Results showed that AJM have significant anti-inflammatory activity and Anti-arthritic Activity in both the doses (200 mg/kg and 400 mg/kg) when compared to the Diclofenac but higher dose was found more effective.Key Words: Anti-inflammatory, Anti-arthritic Activity, Freunds’ complete adjuvant Arthritis, Ajmodadi churna.
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Szabó, Zoltán, and Zoltán Szekanecz. "Arthritis psoriatica." Bőrgyógyászati és Venerológiai Szemle 94, no. 4 (September 4, 2018): 210–14. http://dx.doi.org/10.7188/bvsz.2018.94.4.10.
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Sur, Bongjun, Mijin Kim, Thea Villa, and Seikwan Oh. "Benzylideneacetophenone Derivative Alleviates Arthritic Symptoms via Modulation of the MAPK Signaling Pathway." Molecules 25, no. 15 (July 22, 2020): 3319. http://dx.doi.org/10.3390/molecules25153319.
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The benzylideneacetophenone derivative 3-(4-hydroxy-3-methoxy-phenyl)-1-{3-[1]-phenyl}-propenone (JC3 dimer) was synthesized through the dimerization of JC3. To investigate the inhibitory effects of JC3 dimer, the carrageenan/kaolin (C/K)-induced knee arthritis rat model was used in vivo and rheumatoid arthritis (RA) patient-derived fibroblast-like synoviocytes (FLS) were used in vitro. In the C/K rat model, JC3 dimer was given after arthritis induction for 6 days at the concentrations of 1, 5, or 10 mg/kg/day. Manifestation of arthritis was evaluated using knee thickness, weight distribution ratio (WDR), and squeaking test. The levels of prostaglandin E2 (PGE2), interleukin (IL)-6, and tumor necrosis factor (TNF)-α in the serum of JC3 dimer-treated arthritic rats were also analyzed. Histological examination of the knee joints was also done. For the FLS, the cells were stimulated using IL-1β and concentrations of 1, 5, and 10 μg/mL JC3 dimer were used. The levels of IL-8, IL-6, and PGE2 were measured in stimulated FLS treated with JC3 dimer. At days 5 to 6 after arthritis induction, JC3 dimer treatment significantly decreased arthritic symptoms and reduced the inflammation in the knee joints in the histology of knee tissues in C/K-arthritic rats. In stimulated FLS, JC3 dimer suppressed the increase of IL-8, IL-6, and PGE2. These findings suggest that JC3 dimer has suppressive effects on arthritis, and that JC3 dimer can be a potential agent for arthritis therapy.
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Mian, Syed Shariq, Tajuddin Tajuddin, and Sukirti Upadhyay. "Anti-Arthritic Evaluation of Ginger, Colchicum and Detoxified Nux-Vomica combination for Poly Herbal Unani Formulation." Biomedical and Pharmacology Journal 14, no. 3 (September 30, 2021): 1219–29. http://dx.doi.org/10.13005/bpj/2224.
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Introduction: Arthritis (Wajaul Mafasil) is a condition which is growing worldwide due to lifestyle, environmental and genetic factors. In Unani literature, there are many herbs which are praised for treatment of Arthritis. So polyherbal formulation contains Ginger, Colchicum and Nux- Vomica is taken in combination for arthritis study. This combination is not previously reported but used by unani practitioners. Method: Three crude herbs (Ginger, Colchicum and Nux vomica) were extracted out in both aqueous and hydro-alcoholic solvent. LD-50 of all extracts (aqueous and hydro-alcoholic extract) was determined. Now respective extracts were mixed in effective dose ratio to obtain aqueous and hydro-alcoholic dosage form. Finally both effective combinations (aqueous and hydro-alcoholic) convert into tablet dosage form to determine its anti-arthritic activity by Carrageenan Induced Oedema Test, Cotton Pellet Induced Granuloma Test and Freund’s adjuvant Induced Arthritis Test. The efficacy of the Unani formulation was compared with reference drug (Diclofenac sodium). Result and Discussion: in Carrageenan Oedema Test, animals in high dose hydro-alcoholic, shows decrease in paw volume significantly after 3 hours of Carrageenan injection. In Cotton Pellet Induced Granuloma Test, animals in high dose hydro-alcoholic, shows reduction in granuloma formation significantly. In Freund’s Adjuvant Induced Arthritis Test, The significant reduction in paw volume was found in high dose hydro-alcoholic. Conclusion: Conclusively this study establishes anti-arthritic potential of polyherbal extract in unani literature. Thus these drugs possess synergistic anti-arthritic potential in combination against acute, sub-acute as well as chronic arthritis. So in future compatible dosages form may be prepared for treating arthritis.
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Castillero, Estíbaliz, Ana Isabel Martín, Maria Paz Nieto-Bona, Carmen Fernández-Galaz, María López-Menduiña, María Ángeles Villanúa, and Asunción López-Calderón. "Fenofibrate administration to arthritic rats increases adiponectin and leptin and prevents oxidative muscle wasting." ENDOCRINE CONNECTIONS 1, no. 1 (July 2012): 1–12. http://dx.doi.org/10.1530/ec-12-0003.
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Chronic inflammation induces skeletal muscle wasting and cachexia. In arthritic rats, fenofibrate, a peroxisome proliferator-activated receptor α (PPARα (PPARA)) agonist, reduces wasting of gastrocnemius, a predominantly glycolytic muscle, by decreasing atrogenes and myostatin. Considering that fenofibrate increases fatty acid oxidation, the aim of this study was to elucidate whether fenofibrate is able to prevent the effect of arthritis on serum adipokines and on soleus, a type I muscle in which oxidative metabolism is the dominant source of energy. Arthritis was induced by injection of Freund's adjuvant. Four days after the injection, control and arthritic rats were gavaged daily with fenofibrate (300 mg/kg bw) or vehicle over 12 days. Arthritis decreased serum leptin, adiponectin, and insulin (P<0.01) but not resistin levels. In arthritic rats, fenofibrate administration increased serum concentrations of leptin and adiponectin. Arthritis decreased soleus weight, cross-sectional area, fiber size, and its Pparα mRNA expression. In arthritic rats, fenofibrate increased soleus weight, fiber size, and Pparα expression and prevented the increase in Murf1 mRNA. Fenofibrate decreased myostatin, whereas it increased MyoD (Myod1) and myogenin expressions in the soleus of control and arthritic rats. These data suggest that in oxidative muscle, fenofibrate treatment is able to prevent arthritis-induced muscle wasting by decreasing Murf1 and myostatin expression and also by increasing the myogenic regulatory factors, MyoD and myogenin. Taking into account the beneficial action of adiponectin on muscle wasting and the correlation between adiponectin and soleus mass, part of the anticachectic action of fenofibrate may be mediated through stimulation of adiponectin secretion.
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Setiadi, Anselmus Yakobus Lukita Adiandra, Listya Utami Karmawan, and Yanti Yanti. "Anti-Arthritic and Anti-Inflammatory Effects of Andaliman Extract and Nanoandaliman in Inflammatory Arthritic Mice." Foods 11, no. 22 (November 10, 2022): 3576. http://dx.doi.org/10.3390/foods11223576.
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Inflammatory arthritis is a severe joint disease that causes long-lasting pain that reduces a patient’s quality of life. Several commercial medicines have been used to reduce the inflammation in arthritis. However, they have side effects that affect other organs and increase the infection rate in the patient. Therefore, searching for alternative medicines from natural herbs to use as a substitute for chemical drugs and reduce the side effects of drugs has become the focus of investigation. Zanthoxylum acanthopodium DC., known as andaliman, is an endemic spice that originates from Tapanuli, North Sumatera (Indonesia). Our previous study confirmed that andaliman exerts anti-inflammatory and xanthin oxidase enzymatic inhibitory activities. Unfortunately, there are no in vivo studies on the efficacy of andaliman in reducing inflammation in arthritis. This research aimed to produce an andaliman extract rich in essential oils, to formulate andaliman extract in a nanoemulsion product, and to test their anti-arthritic and anti-inflammatory effects on suppressing the gene expression of inflammatory arthritis in vivo. Several steps were used to conduct this experiment, including andaliman extraction, bioactive compound identification, nanoandaliman formulation, in vivo inflammatory arthritis mice modeling using complete Freund’s adjuvant (CFA), and gene expression quantification using quantitative PCR (qPCR). Andaliman extract and nanoandaliman effectively reduced arthritic scores in CFA-induced arthritic mice. Both treatments also demonstrated anti-inflammatory potential via blocking several arthritic inflammatory gene expressions from cartilage tissue and brain in CFA-induced mice. Nanoandaliman at low dose (25 mg/kg bw) exerted a higher suppressive effect against the gene expression of cox-2, il-ib, inos, and mmp-1 compared to that of andaliman extract. At high dose (100 mg/kg bw), andaliman extract effectively inhibited the expression of il-ib, inos, and mmp-1 genes in arthritic mice. These data suggest that nanoandaliman may be an alternative, natural anti-arthritic and anti-inflammatory candidate for the management of inflammatory arthritis.
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ZANONI, Jacqueline Nelisis, and Gleison Daion PIOVEZANA BOSSOLANI. "DOES THE RHEUMATOID ARTHRITIS AFFECT THE ENTERIC NERVOUS SYSTEM?" Arquivos de Gastroenterologia 56, no. 2 (June 2019): 113–17. http://dx.doi.org/10.1590/s0004-2803.201900000-24.
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ABSTRACT BACKGROUND: Few studies regarding arthritic diseases have been performed to verify the presence of the neurodegeneration. Given the increased oxidative stress and extra-articular effects of the rheumatoid arthritis, the gastrointestinal studies should be further investigated aiming a better understanding of the systemic effects the disease on enteric nervous system. OBJECTIVE: To determine whether the rheumatoid arthritis affects the nitrergic density and somatic area of the nNOS- immunoreactive (IR) myenteric neurons, as well as the morphometric areas of CGRP and VIP-IR varicosities of the ileum of arthritic rats. METHODS: Twenty 58-day-old male Holtzmann rats were distributed in two groups: control and arthritic. The arthritic group received a single injection of the Freund’s Complete Adjuvant in order to induce arthritis model. The whole-mount preparations of ileum were processed for immunohistochemistry to VIP, CGRP and nNOS. Quantification was used for the nitrergic neurons and morphometric analyses were performed for the three markers. RESULTS: The arthritic disease induced a reduction 6% in ileal area compared to control group. No significant differences were observed in nitrergic density comparing both groups. However, arthritic group yielded a reduction of the nitrergic neuronal somatic area and VIP-IR varicosity areas. However, an increase of varicosity CGRP-IR areas was also observed. CONCLUSION: Despite arthritis resulted in no alterations in the number of nitrergic neurons, the retraction of ileal area and reduction of nitrergic somatic and VIP-IR varicosity areas may suggest a negative impact the disease on the ENS.
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Luo, Wenyi, Huilan Yu, Zuhua Cao, Trenton R. Schoeb, Michele Marron, and Kevin Dybvig. "Association of Mycoplasma arthritidis Mitogen with Lethal Toxicity but Not with Arthritis in Mice." Infection and Immunity 76, no. 11 (September 8, 2008): 4989–98. http://dx.doi.org/10.1128/iai.00667-08.
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ABSTRACT Mycoplasma arthritidis induces an acute to chronic arthritis in rodents. Arthritis induced in mice histologically resembles human rheumatoid arthritis and can be associated with lethal toxicity following systemic injection. The M. arthritidis mitogen (MAM) superantigen has long been implicated as having a role in pathogenesis, but its significance with respect to toxicity and arthritogenicity in mycoplasma-induced disease is unclear. To study the pathogenic significance of MAM, M. arthritidis mutants that overproduced or failed to produce MAM were developed. MAM overproduction and knockout mutants were more and less mitogenic, respectively, than the wild-type strain. The degree of mitogenic activity correlated with lethal toxicity in DBA/2J mice. In contrast, histopathological studies detected no correlation between MAM production and the severity of arthritis induced in DBA/2J and CBA/J mice.
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Phadke, K., D. G. Carlson, B. D. Gitter, and L. D. Butler. "Role of interleukin 1 and interleukin 2 in rat and mouse arthritis models." Journal of Immunology 136, no. 11 (June 1, 1986): 4085–91. http://dx.doi.org/10.4049/jimmunol.136.11.4085.
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Abstract The production of interleukin 1 (IL 1) and interleukin 2 (IL 2) by macrophages and lymphocytes from three animal models commonly used for rheumatoid arthritis, viz. adjuvant-induced and type II collagen-induced rat arthritis, and MRL/1 murine arthritis was studied. Although the peritoneal macrophages from adjuvant-arthritic rats in culture produced increased amounts of prostaglandin E2 (PGE2) and lower levels of IL 1 than the control group, cells from collagen-arthritic rats released normal levels of PGE2, but increased amounts of IL 1. After activation with lipopolysaccharides, the IL 1 production by macrophages from all groups was comparable. Addition of indomethacin did not significantly change the IL 1 production in any of these groups. In the absence of any exogenous mitogen, IL 2 production by the lymphocytes of adjuvant-arthritic rats was low, but could be restored to the normal levels when phytohemagglutinin A (PHA) or concanavalin A (Con A) was added. The lymphocytes from collagen-arthritic rats were capable of producing IL 2 without the need of any T cell mitogen. The lymphocytes from MRL/1 mice seemed to lack the functionality in terms of IL 2 production. The macrophagic IL 1 production in these animals was normal. Our data suggest that the type II collagen arthritis model may closely resemble human rheumatoid arthritis in which IL 1 and IL 2 production by the mononuclear cells is significantly enhanced.
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Alshehri, Sultan, Shareefa A. AlGhamdi, Amira M. Alghamdi, Syed Sarim Imam, Wael A. Mahdi, Mohammad A. Almaniea, Baraa Mohammed Hajjar, Fahad A. Al-Abbasi, Nadeem Sayyed, and Imran Kazmi. "Protective effect of fustin against adjuvant-induced arthritis through the restoration of proinflammatory response and oxidative stress." PeerJ 11 (July 26, 2023): e15532. http://dx.doi.org/10.7717/peerj.15532.
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Rheumatoid arthritis causes irreparable damage to joints. The present research sought to check fustin’s anti-arthritic efficacy against the complete Freund’s adjuvant-induced arthritis paradigm in animals by altering the inflammatory response. In the rats, complete Freund’s adjuvant was used to trigger arthritis and they received fustin at 50 and 100 mg/kg for 21 days. At regular intervals, the hind paw volume and arthritic score were assessed. After the trial period, hematological, antioxidant, pro-inflammatory cytokines, and other biochemical parameters were estimated. Fustin-treated rats showed the down-regulation of hind paw volume, arthritic score, and altered hematological parameters (TLC, DLC (neutrophil, lymphocyte, monocyte, eosinophil, basophil)). Furthermore, fustin significantly mitigates proinflammatory cytokine (reduced interleukin, tumor necrosis factor-a (TNF-α), IL-6, IL-1β), oxidative stress (attenuated malondialdehyde (MDA), catalase (CAT), glutathione (GSH), superoxide dismutase (SOD)), attenuated production of prostaglandin E2 and myeloperoxidase (MPO) and improved nuclear factor erythroid 2-related factor (Nrf2) action. Fustin led to the benefit in arthritis-prone animals elicited by complete Freund’s adjuvant via pro-inflammatory cytokine.
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Raghu, Harini, Malinda D. Frederick, Alice Jone, Kathryn E. Talmage, Keith W. Kombrinck, and Matthew J. Flick. "Plasminogen Mediates Both Positive and Negative Effects on Disease Severity in a Mouse Model of TNFα-Driven Arthritis." Blood 118, no. 21 (November 18, 2011): 854. http://dx.doi.org/10.1182/blood.v118.21.854.854.
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Abstract Abstract 854 Rheumatoid arthritis is a chronic inflammatory disease of joint tissue wherein dysregulated, robust hemostatic system activity is a consistent pathological feature. Increased local expression of fibrinolytic system components (i.e., plasminogen activators) and accumulation of fibrin degradation products within arthritic joints suggest that plasmin(ogen) may directly or indirectly participate in joint tissue inflammatory/degradative processes. To test the hypothesis that plasmin-mediated proteolysis drives local events in arthritis pathogenesis, we examined the effect(s) of plasminogen deficiency (Plg−) on TNFα-driven arthritis in Tg197 transgenic mice that spontaneously develop a chronic, erosive form of polyarthritis. Comparative macroscopic analysis of the distal joints (fore- and hind-paws) from 10-week old mice revealed that plasminogen deficiency resulted in significantly elevated arthritic disease compared to plasminogen-sufficient control animals. Consistent with overt macroscopic disease, evaluation of distal joint sections using a semi-quantitative histopathological scoring system confirmed that Plg− Tg197 mice developed significantly more advanced arthritic disease relative to controls. Typical disease features included extensive synovial hyperplasia, inflammatory cell infiltration, pannus formation, cartilage degradation and bone loss. Remarkably, histological examination of the proximal joints (knees) from the same set of animals revealed that Plg− Tg197 mice developed markedly diminished arthritic disease relative to controls, suggesting that the impact of plasminogen on the progression of arthritis is dependent on anatomical location. Given that fibrin is a primary substrate for plasmin-mediated proteolysis, we examined joint tissue for evidence of fibrin deposition by immunohistochemistry. In distal joints of the paws, Plg− Tg197 mice displayed robust fibrin deposition throughout the hyperplastic synovial tissue and along the articular surfaces exhibiting evidence of cartilage degradation. The degree of fibrin staining in the distal paw joints appeared to correlate with the disease severity (i.e., more extensive fibrin staining in Plg− Tg197 mice with advanced arthritic disease). Intriguingly, fibrin deposition was also observed in the proximal knee joints of Plg− Tg197 transgenic mice, despite the limited arthritis severity. To determine whether fibrin was the plasmin substrate mediating the distinct differences in TNFα-driven arthritis severity at one or both of the anatomical locations examined (i.e., paw joints or knee joints) in Plg− Tg197 mice, fibrinogen deficiency was superimposed on the Plg− background generating mice with combined plasminogen and fibrinogen deficiencies (e.g., Plg−/Fib− mice). Remarkably, comparative macroscopic as well as microscopic analyses revealed that the arthritis phenotypes were reversed in both the paw and the knee joints of Plg−/Fib− Tg197 mice relative to Plg−/Fib+ Tg197 mice. Together, these data strongly suggest that fibrin is a dominant plasmin target that contributes to arthritis pathogenesis. A thorough understanding of the precise mechanisms underlying the plasminogen-dependent, location-specific differences in arthritis progression will likely provide valuable insight into novel therapeutic strategies to effectively treat inflammatory arthritis. Disclosures: No relevant conflicts of interest to declare.
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Granado, Miriam, Teresa Priego, Ana I. Martín, M. Ángeles Villanúa, and Asunción López-Calderón. "Anti-inflammatory effect of the ghrelin agonist growth hormone-releasing peptide-2 (GHRP-2) in arthritic rats." American Journal of Physiology-Endocrinology and Metabolism 288, no. 3 (March 2005): E486—E492. http://dx.doi.org/10.1152/ajpendo.00196.2004.
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Chronic arthritis induces hypermetabolism and cachexia. Ghrelin is a gastrointestinal hormone that has been proposed as a treatment to prevent cachexia. The aim of this work was to examine the effect of administration of the ghrelin agonist growth hormone-releasing peptide-2 (GHRP-2) to arthritic rats. Male Wistar rats were injected with Freund’s adjuvant, and 15 days later arthritic and control rats were daily injected with GHRP-2 (100 μg/kg) or with saline for 8 days. Arthritis induced an increase in serum ghrelin ( P < 0.01) and a decrease in serum concentrations of leptin ( P < 0.01), whereas GHRP-2 administration increased serum concentrations of leptin. GHRP-2 increased food intake in control rats but not in arthritic rats. However, in arthritic rats GHRP-2 administration ameliorated the external symptoms of arthritis, as it decreased the arthritis score (10.4 ± 0.8 vs. 13.42 ± 0.47, P < 0.01) and the paw volume. In addition, circulating IL-6 and nitrites/nitrates were increased by arthritis, and GHRP-2 treatment decreased the serum IL-6 levels ( P < 0.01). To elucidate whether GHRP-2 is able to modulate IL-6 release directly on immune cells, peritoneal macrophage cultures were incubated with GHRP-2 or ghrelin, the endogenous ligand of the growth hormone (GH) secretagogue receptor. Both GHRP-2 (10−7 M) and ghrelin (10−7 M) prevented endotoxin-induced IL-6 and decreased nitrite/nitrate release from peritoneal macrophages in vitro. These data suggest that GHRP-2 administration has an anti-inflammatory effect in arthritic rats that seems to be mediated by ghrelin receptors directly on immune cells.
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Parmar, Deepika, Neetesh Kumar Jain, and Vivek Tomar. "Anti-arthritic Evaluation of Different Extracts of Boerhaavia diffusa Linn. in FCA Induced Arthritis In Rats." Journal of Drug Delivery and Therapeutics 8, no. 5-s (October 15, 2018): 388–93. http://dx.doi.org/10.22270/jddt.v8i5-s.1922.
Full textAbstract:
The main aim of study is to evaluate the anti-arthritic effect of different extracts of Boerhaavia diffusa in arthritic rats. Different extracts were prepared by successive solvent extraction methods by using the various polar and non polar solvents and their % yields were calculated. Arthritis was induced by FCA induced arthritis model in rats and paw volume was measured on different days. Body weights of all animals were also measured simultaneously and at the end of experiment some haematological parameters were measured. On preliminary phytochemical studies extracts showed the presence of alkaloids, fatty acids, terpenoids, flavonoids and phenolic compounds. Among all extracts, methanolic extract significantly decreased the paw volume in all treated groups. Methanolic extracts also restored the body weight significantly. The results of our study revealed that all the extracts treated group’s causes significant alterations in the hematological parameters and maximal effects were observed at 400 mg/kg. Since methanolic extract showed best activity in arthritic model and its phytochemical study showed presence of flavonoids and phenolic compounds, so it may be possible that anti-arthritic activity of root extracts may be due to presence flavonoids.
Keywords: Arthritis, FCA induced arthritis, Boerhaavia diffusa, haematological parameters, and Body weight
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Rajashekar Perusomula, Shruthi Thamannagari, Gayathri Paturi, and Ramesh Alluri. "Evaluation of anti-arthritic activity of Hyptis suaveolens seeds in rats." GSC Biological and Pharmaceutical Sciences 27, no. 3 (June 30, 2024): 077–98. http://dx.doi.org/10.30574/gscbps.2024.27.3.0225.
Full textAbstract:
Rheumatoid arthritis has been treated with Hyptis suaveolens (L) poit. seeds. There has been no pharmaceutical assessment for rheumatoid arthritis. A study aims to assess the anti-arthritic properties of aqueous extract of Hyptis suaveolens (L) poit… seeds (AEHS). Standard techniques were used for phytochemical analysis. Tested anti-arthritic potential in-vitro (25-800µg/ml egg albumin) and in vivo (200 and 400 mg/kg egg albumin induced arthritic model). Chemicals such alkaloids, sugars, flavonoids, phenols, and terpenoids were found. Results showed 75% reduction of protein denaturation at 800µg/ml in-vitro. According to the Egg albumin model, AEHS considerably (P < 0.0001) inhibits changes in paw volume, joint diameter, and body weight. It also improves hematological, biochemical, and histopathological levels. The findings confirm the traditional usage of Hyptis suaveolens(L)poit. seeds to treat rheumatoid arthritis.
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Chen, Jian-Yu, Xiao-Yun Tian, Wen-Jing Liu, Bao-Kun Wu, Yue-Chan Wu, Ming-Xing Zhu, Jin-Liu, et al. "Importance of Gedunin in Antagonizing Rheumatoid Arthritis via Activating the Nrf2/ARE Signaling." Oxidative Medicine and Cellular Longevity 2022 (April 7, 2022): 1–18. http://dx.doi.org/10.1155/2022/6277760.
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Objective. This study assessed the anti-arthritic effect and protection of Gedunin (GDN) on joint tissues and revealed the possible mechanism in suppressing rheumatoid arthritis (RA). Methods. LPS-induced macrophages and TNF-α-stimulated synovial fibroblasts (MH7A) or IL-1β-stimulated primary rheumatoid arthritis synovial fibroblasts (RASFs) were used to evaluate the antiinflammatory effect of GDN. In addition, CIA-induced arthritis was employed here to evaluate the anti-arthritic effect. MTT and BRDU assays were utilized to evaluate the cell viability and proliferation, Q-PCR was conducted to detect the mRNA expression of cytokines, FACS was adopted to monitor ROS production, while western blotting (WB) and siRNA interference were applied in confirming the anti-arthritic effects of GDN via the Nrf2 signaling. Results. In vitro, cell viability was inhibited in macrophages and MH7A cells, but not in RASFs; but the proliferation of RASFs was significantly suppressed in time- and dose-dependent manners. GDN suppressed cytokine levels in LPS-stimulated macrophages and TNF-α-stimulated MH7A cells or RASFs. GDN suppressed ROS expression. Furthermore, GDN treatment notably dose-dependently decreased the mRNA and protein expression of iNOS in LPS-induced macrophages. sip62 interference results showed that GDN cause the less expression of HO-1 and Keap1 and also fail to inhibit cytokines after sip62 interference. In vivo, GDN effectively inhibited paw swelling, arthritis score, and arthritis incidence and cytokines. Conclusions. Our study suggested that GDN exhibited strong antagonistic effect on arthritis both in vitro and in vivo via activation of Nrf2 signaling. Our work will provide a promising therapeutic strategy for RA.
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Gouze, Jean-Noel, Steven C. Ghivizzani, Elvire Gouze, Glyn D. Palmer, Oliver B. Betz, Paul D. Robbins, Christopher H. Evans, and James H. Herndon. "GENE THERAPY FOR RHEUMATOID ARTHRITIS." Hand Surgery 06, no. 02 (December 2001): 211–19. http://dx.doi.org/10.1142/s0218810401000709.
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Advances in understanding the biology of rheumatoid arthritis (RA) have opened new therapeutic avenues. One of these, gene therapy, involves the delivery to patients of genes encoding anti-arthritic proteins. This approach has shown efficacy in animal models of RA, and the first human, phase I trial has just been successfully completed. Hand surgery featured prominently in this pioneering study, as a potentially anti-arthritic gene encoding the interleukin-1 receptor antagonist was transferred to the metacarpophalangeal joints of subjects with RA one week before total joint arthroplasty. This study has confirmed that it is possible to transfer genes safely to human joints. It should pave the way for additional application of gene therapy to arthritis and other orthopaedic conditions.
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Ma, Ying, Kathleen Petri Seiler, Ernst J. Eichwald, John H. Weis, Cory Teuscher, and Janis J. Weis. "Distinct Characteristics of Resistance toBorrelia burgdorferi-Induced Arthritis in C57BL/6N Mice." Infection and Immunity 66, no. 1 (January 1, 1998): 161–68. http://dx.doi.org/10.1128/iai.66.1.161-168.1998.
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ABSTRACT Studies of mice infected with Borrelia burgdorferi have indicated that the severity of arthritis is influenced by the genetic composition of the host: the C3H mouse develops severe arthritis while BALB/c and C57BL/6 mice develop mild arthritis. In this study, the effects of increasing infectious dose on the severity of arthritis were determined in these three mouse strains. C3H/He mice developed severe arthritis at all infectious doses, with 100% infection requiring 200 spirochetes. In BALB/cAnN mice, arthritis severity was dependent on infectious dose; symptoms were mild with infection by 200 B. burgdorferi and progressively more severe with increasing infectious dose. Infection of BALB/cAnN mice with 2 × 104 B. burgdorferi resulted in arthritis with severity identical to that in C3H/He mice. Spirochete levels in rear ankle joints of C3H/HeJ and C3H/HeN mice were relatively high, as detected by PCR, and did not increase with infectious dose. Spirochete levels in joints from BALB/cAnN mice increased with increasing infectious dose to levels found in severely arthritic C3H/He mice. Thus, resistance to severe arthritis in BALB/cAnN mice was conditional: it could be overcome by high infectious dose and the arthritis became severe when high levels of B. burgdorferi were present in joints. A unique response to increasing infectious dose was seen in C57BL/6N mice, which displayed mild to moderate arthritis at all doses of B. burgdorferi tested, up to 2 × 105. At all infectious doses, the levels of spirochetes in ankle joints of C57BL/6N mice were high, equivalent to those found in the severely arthritic C3H/He mice. The arthritis observed in infected (C57BL/6N × C3H/HeN)F1 mice was of severity intermediate between those of the two parental strains. The finding that resistance to severe arthritis in C57BL/6N mice could not be overcome by high infectious doses and was independent of spirochete levels in joints suggested that it was mediated by a distinct mechanism from that operating in BALB/cAnN mice.
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Mobashar, Aisha, Arham Shabbir, Muhammad Shahzad, and Saeed-ul-Hassan. "Evaluation of Immunomodulatory and Antiarthritic Potential of Trigonella gharuensis Extracts." Evidence-Based Complementary and Alternative Medicine 2020 (December 12, 2020): 1–7. http://dx.doi.org/10.1155/2020/8836080.
Full textAbstract:
The genus of Trigonella has long been used for the treatment of arthritis and inflammatory disorders. This study was aimed to investigate the immunomodulatory activities of ethanol and n-hexane extracts of T. gharuensis in the rat model of rheumatoid arthritis. Freund’s complete adjuvant (FCA) model was used to induce arthritis in rats. Arthritis was induced on day 0, while treatment which was started on day 8 continued for twenty days. Arthritic development and paw edema were determined using an arthritic scoring index and plethysmometer, respectively. Histopathology was evaluated using H&E staining. RNA extraction, reverse transcription, and polymerase chain reaction (RT-PCR) were performed to determine expression levels of proinflammatory markers such as TNF-α, NF-ĸB, IL-6, IL-1β, COX2, and anti-inflammatory cytokine IL-4. Prostaglandin E2 level (PGE2) was evaluated using ELISA. Blood analysis and biochemical parameters were also determined. The significance level was set as P < 0.05 . Treatment with extracts reduced paw edema, arthritic progression, and histopathological parameters. Expression levels of abovementioned proinflammatory cytokines and COX2 were downregulated, while IL-4 was upregulated. PGE2 levels were found reduced with extract treatment. Blood parameters were nearly normalized in treatment groups. Extract treatment did not alter biochemical parameters. Both extracts had effects comparable with piroxicam. In conclusion, extracts of T. gharuensis ameliorated experimentally induced arthritis that may be ascribed to its immunomodulatory effects.
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Riccio, A., and G. Tarantino. "Hepatitis C Virus-Related Arthtitis and Rheumatoid Arthritis: Could They Be Different Aspects of the Same Disease?" International Journal of Immunopathology and Pharmacology 25, no. 1 (January 2012): 293–96. http://dx.doi.org/10.1177/039463201202500134.
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The role played by HCV in the genesis of many autoimmune disorders has been reported in several studies. In particular, the onset of arthritis has been described in about 2–3% of HCV infection cases. At present, this HCV-related arthritis is classified as a reactive arthritis, but a real distinction of this form from classical rheumatoid arthritis is often difficult. In this presentation, the Authors distinguish two arthritic forms observed in HCV-related arthritis patients: one, characterized by asymmetrical oligoarticular-involvement, and another, with poly-articular symmetrical involvement. The Authors suggest that the latter can be considered as a form of rheumatoid arthritis, because of the similarity of the main clinical aspects and laboratory findings (rheumatoid factor, anti-cyclic citrullinated peptide antibodies) to those of classical rheumatoid arthritis, which make the two forms indistinguishable. Therefore, HCV could be considered the etiologic agent of a limited number of cases of rheumatoid arthritis.
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Brown, Charles R., and Steven L. Reiner. "Clearance of Borrelia burgdorferi May Not Be Required for Resistance to Experimental Lyme Arthritis." Infection and Immunity 66, no. 5 (May 1, 1998): 2065–71. http://dx.doi.org/10.1128/iai.66.5.2065-2071.1998.
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ABSTRACT Infection of inbred mouse strains with Borrelia burgdorferi results in the development of experimental Lyme arthritis. The degree of arthritic pathology has been suggested to correlate with the level of spirochete burden within tissues. To investigate this further, we infected resistant DBA/2 (DBA) and susceptible C3H/HeJ (C3H) mice in the hind footpads and monitored arthritis development for 21 days. To quantitate levels of spirochetes within tissues, we created a competitive PCR molecule containing modified ospA and fla gene segments. C3H mice developed severe arthritis of the tibiotarsal joints, while DBA mice developed only mild inflammation throughout the experimental period. At day 21, when the gross size and histologic composition of ankles revealed significant differences in arthritis between the strains, there was little difference in levels of spirochete DNA as determined by competitive PCR. Cultures of ankle tissue at day 21 were also uniformly positive in both C3H and DBA animals and contained relatively similar levels of spirochetes. These results indicate that the presence of spirochetes in the ankles of experimental animals is not sufficient for arthritis development. Since arthritic and nonarthritic animals can harbor relatively equal spirochete burdens yet retain their distinct phenotypic outcomes, an aberrant or overly exuberant immune response may be an additional requirement for pathology in arthritis-prone mice.
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Ramez, Mohamed, Toni Forde, Chi-Wing Chow, and Vyacheslav Adarichev. "Genome-wide association study of inbred murine strains discovered nuclear factor of activated T-cells Nfatc4 as a major gene controlling severity of inflammatory arthritis. (47.14)." Journal of Immunology 186, no. 1_Supplement (April 1, 2011): 47.14. http://dx.doi.org/10.4049/jimmunol.186.supp.47.14.
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Abstract Nuclear factor of activated T cells (NFAT) is a family of transcription factors critical in regulating gene expression in development and disease. NFAT is an important target for cyclosporine immunosuppression in transplant rejection. The NFAT pathway is also important in inflammatory and autoimmune diseases such as rheumatoid arthritis. Using genome-wide association study (GWAS) of antibody-mediated arthritis in inbred murine strains, we found NFATc4 within the major arthritis severity peak at 56.35-56.46 Mb of chromosome 14 with genetic association of log(1/p) > 5.5. To confirm the genetic linkage and functional significance of the NFATc4 gene, we performed collagen antibody-induced arthritis (CAIA) and found that NFATc4-deficient mice exhibited significantly reduced inflammation as compared to wild-type counterparts (55% downregulation, p < 0.01). Immunoblotting analysis demonstrated the presence of NFATc4 in articular cartilage and chondrocytes derived from femoral heads of arthritic and naïve mice. Notably, NFATc4 in chondrocytes isolated from arthritic mice was hypo-phosphorylated as compared to naïve cells, indicating activation of NFATc4. NFATc4, as expected, was not found in splenocytes. We also performed genome-wide Affymetrix oligonucleotide array studies in CAIA experimental arthritis model using wild type and NFATc4-deficient mice. Taking together, we uncovered a novel role of NFATc4 in inflammatory arthritis in chondrocytes.
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Mu, Hong. "In vivo blocking CD80 promotes Th17 polarization and amplifies autoimmune arthritis severity in mice infected with Mycoplasma arthritidis (43.15)." Journal of Immunology 188, no. 1_Supplement (May 1, 2012): 43.15. http://dx.doi.org/10.4049/jimmunol.188.supp.43.15.
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Abstract Mycoplasma arthritidis, an agent that causes acute and chronic autoimmune arthritis and septic shock in rodents. Previously we demonstrated that the severity of septic shock induced in mice injected with M. arthritidis is associated with the up-regulation of co-stimulatory molecule CD80 on APCs and blockade of CD80 specifically enhances the severity of arthritis. In the present study, we report that anti-CD80 resulted in increased number of Th17 T cells and level of IL-23 expression by macrophages resulting in the increased expression and production of IL-17 and augmented Th17-associated transcriptional factors RORgt and Stat3 by CD4+ T cells. Also in arthritis susceptible mouse strain, injection of anti-TLR4 mAb significantly suppresses IL-23 response and IL-17 by CD4+ T cells and alleviate the arthritis. The inhibition of Th17 response by anti-TLR4 treatment is partially associated with the suppression of CD80 function. In addition, to elucidate the role of MAM, the superantigen secreted by M. arthritidis in Th17 polarization, mice injected with MAM-mutant M. arthritidis strains showed impaired IL-17 production, remarkably lower IL-23 and improved arthritis symptoms. Thus the contribution of MAM appears to be important for IL-17 contribution in the disease pathogenesis and is clearly involved in modulating pathways of immune responses leading to different disease outcomes and phenotypes in M. arthritidis-induced autoinflammatory disease.
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BRUOT, BRENT C., and JEFFREY W. CLEMENS. "Regulation of Testosterone Production in the Adjuvant‐Induced Arthritic Rat." Journal of Andrology 13, no. 1 (January 2, 1992): 87–92. http://dx.doi.org/10.1002/j.1939-4640.1992.tb01634.x.
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ABSTRACT: Serum testosterone concentrations are reduced in men with rheumatoid arthritis and in rats with adjuvant‐induced arthritis, a common model for rheumatoid arthritis. To understand the mechanism responsible for this reduction, testosterone production by testicular cells and Percoll‐purified Leydig cells from nonarthritic and arthritic rats was studied. Leydig cells in crude interstitial cell preparations from arthritic rats secreted significantly less testosterone in response to human chorionic gonadotropin (hCG) stimulation than cells from nonarthritic animals. In contrast, no differences in hCG and dibutyryl cyclic adenosine monophosphate‐stimulated testosterone production by Percoll‐enriched Leydig cells from arthritic and nonarthritic animals were observed. To determine whether a secretory product from testicular macrophages was important to this reduction, macrophages from arthritic and nonarthritic animals were cultured. The conditioned media from these cultures were added to cultures of interstitial cells from nonarthritic animals. Nonarthritic rat testicular macrophage‐conditioned medium had no significant effect on testosterone production. In contrast, conditioned medium from arthritic rat testicular macrophages significantly reduced testosterone production. These results suggest that testicular macrophages secrete a factor that may be important in the regulation of testosterone production in the adjuvant‐induced arthritic rat.
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Butz, Daniel E., Guangming Li, Shane M. Huebner, and Mark E. Cook. "A mechanistic approach to understanding conjugated linoleic acid's role in inflammation using murine models of rheumatoid arthritis." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 293, no. 2 (August 2007): R669—R676. http://dx.doi.org/10.1152/ajpregu.00005.2007.
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A naturally occurring fatty acid, conjugated linoleic acid (CLA), reduces immune-induced TNF and inducible cyclooxygenase (COX-2) expression; key mediators of inflammation in rheumatoid arthritis (RA). On the basis of previous work, it was hypothesized that dietary CLA would act as an anti-inflammatory agent in select animal models of RA. In the collagen antibody-induced arthritis (CAIA) model, mice fed CLA (mixed isomers of c9, t11, and t10, c12-CLA) for 3 wk before anticollagen antibody injection had reduced lipopolysaccharide-induced plasma TNF levels and had arthritic scores that were 60% of mice fed corn oil (CO). In the collagen-induced arthritis (CIA) model, mice fed mixed isomers of CLA for 21 days before immunization had lower IgG1 titers, earlier signs of joint inflammation, but similar arthritis scores compared with CO fed mice during the remaining 70-day post-injection period. Beginning on day 80 to 133, CLA-fed mice had arthritic scores 70% that of the CO-fed mice. In a second CIA experiment, CLA was fed only after the booster injection. Plasma IgG1 levels were not reduced and arthritis onset was delayed 4 days in CLA-fed mice compared with the CO-fed mice. Peak arthritis score was similar between CLA and CO-fed mice from day 35 to 56. Because CLA reduced inflammation in the CAIA model, delayed onset of arthritis in the CIA model (CIA experiment 2) and reduced arthritis score after day 80 in the CIA model (CIA experiment 1), we concluded that dietary CLA exhibited anti-inflammatory activity that was dependent on antibody.
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Oduro, Kwadwo A., Fang Liu, Qing Tan, Chan-Kyu Kim, Olga Lubman, Daved Fremont, Jason C. Mills, and Kyunghee Choi. "Myeloid skewing in murine autoimmune arthritis occurs in hematopoietic stem and primitive progenitor cells." Blood 120, no. 11 (September 13, 2012): 2203–13. http://dx.doi.org/10.1182/blood-2011-11-391342.
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Abstract Skewing toward myeloid cell production is often observed in chronic inflammation and autoimmune diseases. Herein, we determined whether persistent myeloid activation and proinflammatory output occurring in pathologic conditions is at the level of hematopoietic stem and primitive progenitor cells (HSPPCs). By using a mouse arthritis model, we found that even though HSPPCs in arthritis still retained the capacity to differentiate into different lineages, they acquired enhanced in vitro and in vivo propensity in a disease-dependent manner to generate myeloid cells, the key perpetrators of tissue damage in arthritis. This myeloid skewing was cell intrinsic, as arthritic HSPPCs up-regulate myeloid-specific transcripts including S100a8. Exogenous S100a8 promoted myeloid cell output from wild-type HSPPCs, suggesting mechanistic involvement of this gene in the myeloid priming that occurs in arthritic HSPPCs. Therefore, our results indicate that in arthritic mice, HSPPCs adopt a pathologic state that favors disease persistence.
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Tirupathi Rao Y R K V, Gopal Rao K, and Satishchandra A. "Anti-arthritic evaluation of Eclipta alba in a murine model Freund’s adjuvant provoked arthritis." International Journal of Research in Pharmaceutical Sciences 11, no. 1 (February 4, 2020): 1012–17. http://dx.doi.org/10.26452/ijrps.v11i1.1929.
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Eclipta alba (E.alba) is a medicinal plant with wide range of biological action encompassing antioxidant and anti-inflammatory. However, its anti arthritic activity is not reported till date. So we have evaluated the anti-arthritic property of E.alba methanolic extract in arthritis induced rats. The rats were made arthritic by single intradermal injection of complete freunds adjuvant (CFA) and E.alba (200 and 400mg/kg) were administered for 28 days. The assessment of arthritis was done by evaluating body weight, paw volume and alteration in hematological parameters (WBC, RBC, Hb and ESR). Further, to evaluate oxidative stress, malondialdehyde (MDA), a marker of lipid peroxidation and antioxidants (SOD, CAT, GPx and GSH) were measured. The arthritis induced rats showed significant decrease in body weight, elevated paw oedema, and changes in blood parameters. Treatment with E.alba significantly reduced the arthritic symptoms by its anti-inflammatory effect. Further, arthritic rats displayed elevated MDA and decreased antioxidant levels and treatment with E.alba inhibited the lipid peroxidation and restored the antioxidants to normal. The present study reveals that Eclipta alba showed effective anti-arthritic activity through its antioxidant and anti-inflammatory property. Further the anti-arthritic activity of E. alba might be due to the presence of various phytochemicals such as flavanoids and polyphenols.
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Kim, Hwan Mook, Jong Soon Kang, Ki Hoon Lee, Chang Woo Lee, Kiho Lee, and Song-Kyu Park. "Anti-inflammatory and anti-arthritic effect of essential oil isolated from Curcuma wenyujin (35.7)." Journal of Immunology 184, no. 1_Supplement (April 1, 2010): 35.7. http://dx.doi.org/10.4049/jimmunol.184.supp.35.7.
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Abstract Curcuma species has been reported to exert anti-inflammatory and anti-tumor effects. Curcuma wenyujin is mainly cultivated in wenzhou region of China and it was reported that the main constituents of Curcuma wenyujin is different from that of other Curcuma species. In this study, we investigated the effect of essential oil isolated from Curcuma wenyujin (CW) on inflammation and arthritis in rodents. CW dose-dependently suppressed lipopolysaccharide (LPS)-induced TNF-α production in mice. CW also inhibited zymosan-induced inflammation in concentration-dependent manner. Further studies demonstrated that CW attenuated the development of arthritis in adjuvant- and collagen-induced arthritis model and the anti-arthritic effect of the highest dose of CW was comparable to that of 0.1 mg/kg of dexamethasone. Collectively, the results presented in this report demonstrate that CW exerts anti-inflammatory and anti-arthritic effects. Our results suggest that CW might be a potential therapeutic agent for the treatment of inflammatory diseases, including rheumatoid arthritis.
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Dudics, Steven, Shivaprasad Venkatesha, and Kamal Moudgil. "The Micro-RNA Expression Profiles of Autoimmune Arthritis Reveal Novel Biomarkers of the Disease and Therapeutic Response." International Journal of Molecular Sciences 19, no. 8 (August 5, 2018): 2293. http://dx.doi.org/10.3390/ijms19082293.
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Rheumatoid arthritis (RA) is a chronic autoimmune disease of the joints affecting about 0.3–1% of the population in different countries. About 50–60 percent of RA patients respond to presently used drugs. Moreover, the current biomarkers for RA have inherent limitations. Consequently, there is a need for additional, new biomarkers for monitoring disease activity and responsiveness to therapy of RA patients. We examined the micro-RNA (miRNA) profile of immune (lymphoid) cells of arthritic Lewis rats and arthritic rats treated with celastrol, a natural triterpenoid. Experimental and bioinformatics analyses revealed 8 miRNAs (miR-22, miR-27a, miR-96, miR-142, miR-223, miR-296, miR-298, and miR-451) and their target genes in functional pathways important for RA pathogenesis. Interestingly, 6 of them (miR-22, miR-27a, miR-96, miR-142, miR-223, and miR-296) were further modulated by celastrol treatment. Interestingly, serum levels of miR-142, miR-155, and miR-223 were higher in arthritic versus control rats, whereas miR-212 showed increased expression in celastrol-treated rats compared with arthritic rats or control rats. This is the first study on comprehensive miRNA expression profiling in the adjuvant-induced arthritis (AA) model and it also has revealed new miRNA targets for celastrol in arthritis. We suggest that subsets of the above miRNAs may serve as novel biomarkers of disease activity and therapeutic response in arthritis.