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Chiou, CF, L. Wanke, E. Yu, and J. Ofman. "AR2 A COST-EFFECTIVENESS ANALYSIS OF BIOLOGICAL TREATMENTS FOR RHEUMATOID ARTHRITI ARTHRITIS." Value in Health 7, no. 3 (May 2004): 223. http://dx.doi.org/10.1016/s1098-3015(10)62076-1.
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Ning, Qiaoyi, Xueming Yao, Ying Huang, Lei Hou, Daomin Lu, Yutao Yang, Yamei Zhan, Yiting He, and Wukai Ma. "3-O-Caffeoylquinic acid in Periploca forrestii Schltr extract ameliorates collagen-induced arthritis by inducing IL17/IL23 cells in rats." Tropical Journal of Pharmaceutical Research 21, no. 7 (August 21, 2022): 1445–52. http://dx.doi.org/10.4314/tjpr.v21i7.13.
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Purpose: To study the therapeutic effect of 3-O-caffeoylquinic acid (3-O-CQA) from Periploca forrestii extract (PFE) on collagen-mediated arthritis (CIA) in rats, as well as the potential underlying mechanism of action.
Methods: PFE and 3-O-CQA were successively and intragastrically administered to CIA rats. Paw swelling, arthritic scores and H & E staining were used to evaluate the therapeutic effect of 3-O-CQA. Moreover, to determine the effects of PFE and 3-O-CQA on fibroblast-resembling synoviocytes obtained from arthritic subjects (RAFLS), the viability of RAFLS cultured in vitro was measured with MMT, while apoptotic lesions were analyzed by flow cytometry. The levels of IL-6 in CIA and RAFLS were determined by enzyme-linked immunosorbent assay (ELISA), while quantitative reverse transcriptionpolymerase chain reaction (qRT-PCR) and immunoblotting were used to assess their mRNA and
polypeptide levels, respectively.
Results: PFE in 3-O-CQA ameliorated swelling and reduced arthritic scores in CIA rat model, and also decreased cytokine levels (p < 0.05). By decreasing mRNA and protein expressions, 3-O-CQA repressed the phosphorylation of STAT3 and JAK2 as well as the protein levels of IL-23 and RORγt (p < 0.05).
Conclusion: The results of this study show that CIA and RAFLS are ameliorated in rats by 3-O-CQA in PFE through regulation of IL17/ IL23 and Th17 cells. Thus, 3-O-CQA affords a therapeutic strategy for the management of collagen-induced arthritis.
Keywords: Arthriti; Periploca forrestii Schltr extract; 3-O-Caffeoylquinic acid; Interleukin (IL)-17; IL-23; Th17 cells
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Al-Samman, Deena, Nashwan Al-Asaady, and Salem Al-Jader. "Combination Therapy with Rituximab and Methotrexate in the Management of Rheumatoid Arthriti." Annals of Tropical Medicine and Public Health 22, no. 10 (2019): 128–34. http://dx.doi.org/10.36295/asro.2019.221019.
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Francisco, Charo. "Close Family Ties: Familial Interstitial Lung Disease Secondary to Familial Juvenile Idiopathic Arthriti." Chest 142, no. 4 (October 2012): 458A. http://dx.doi.org/10.1378/chest.1389005.
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Desi, Desi. "TATUS KESEHATAN MENTAL PASIEN GOUT ARHTRITIS DI KOTA TOMOHON." Jurnal Kesehatan Bakti Tunas Husada: Jurnal Ilmu-ilmu Keperawatan, Analis Kesehatan dan Farmasi 19, no. 2 (September 9, 2019): 226. http://dx.doi.org/10.36465/jkbth.v19i2.501.
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<span class="fontstyle0">Gout Arthritis </span><span class="fontstyle0">is a disease known as gout, but in certain conditions this disease can cause physical<br />symptoms that are not visible to some people. When there are problems with physical health, other<br />health aspects will also have an impact. The same is true for patients diagnosed with </span><span class="fontstyle0">Gout Arthritis</span><span class="fontstyle0">,<br />not only physical aspects but can affect other aspects, especially when having physical symptoms such<br />as tofi. Mental health is a condition where there is a balance between emotional, behavioral and<br />cognitive. This is the basis of the importance of maintaining mental health for someone who does not<br />have physical health problems and for someone who has a disease such as </span><span class="fontstyle0">Gout Arthritis </span><span class="fontstyle0">patients. The<br />purpose of this study was to find out how mental health status in </span><span class="fontstyle0">Gout Arthritis </span><span class="fontstyle0">patients in Tomohon<br />City. Quantitative research using a descriptive approach was used in this study. Data collection used<br />survey methods with questionnaires. The results showed that the majority of respondents had adequate<br />mental health (80.6%). Based on the results of the study, it was concluded that mental health status in<br /></span><span class="fontstyle0">Gout Arthriti</span><span class="fontstyle0">s patients in Tomohon City was at a sufficient level. These influenced by himself and the<br />environment around them.</span> <br /><br />
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Zuber, Z., K. Kasperkiewicz, M. Michalski, Ł. Eppa, M. Bartłomiejczyk, A. Świerzko, E. Mężyk, M. Noszczyńska, and M. Cedzyński. "THU0537 Selected Factors of Complement Lectin Pathway Factors in Polish Children with Juvenile Idiopathic Arthriti." Annals of the Rheumatic Diseases 74, Suppl 2 (June 2015): 394.3–395. http://dx.doi.org/10.1136/annrheumdis-2015-eular.4204.
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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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Bogmat, Ludmila, Anastasia Fadeeva, Nataliya Shevchenko, and Viktoria Nikonova. "The state of physical functionning of patients with juvenile idiopathic arthritis in the assessment of quality of life." 8, no. 8 (December 29, 2021): 11–21. http://dx.doi.org/10.26565/2617-409x-2021-8-01.
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Summary. Juvenile idiopathic arthritis is a severe chronic childhood disease that affects not only the joints but is also accompanied by various comorbid conditions, among which eye damage (uveitis) is the most common. In addition to a significant impact on the general condition of the child, this disease also affects the main indicators of quality of life: physical activity, emotional activity, activity in educational institutions, and the social sphere. During the period of active study of Juvenile idiopathic arthritis patients quality of life, a decrease in its overall level is noted due to almost all components, but physical activity shows the lowest values in some studies, which is associated with joint damage, activity, and duration of the disease. Objective. To determine the state of physical functioning and assess the overall level of quality of life in patients with JIA, considering the subtype of the disease duration and the therapy complex. Materials and Methods. The study was carried out at SI "Institute for Children and Adolescents Health Care of the NAMS of Ukraine", Kharkiv, from November 2020 till November 2021. There 118 patients with juvenile idiopathic arthritis were examined, including 47 with polyarticular, 43 with oligoarticular, 28 with uveitis-associated subtypes. The investigation involved 77 girls and 41 boys in age from 2 till 18 years old. The therapy by methotrexate was provided in 111 patients, among them 30 had methotrexate with immunobiological therapy (29 adalimumab, 1 – tocilizumab), 6 – sulfasalazine. The disease duration due to disease subtype was in children with polyarthritis – (49,2±6,7), oligoarthritis – (35,4±4,2), uveitis-associated subtypes of juvenile idiopathic arthritis – (76,8±10,2) months. Disease activity was assessed using the Juvenile Arthritis Disease Activity Score 27-joint reduced count questionnaire, functional state according to he Child Health Assessment Questionnaire and quality of life according to PedsQLTM 4.0 Generic Core Scales. Results. It was found that high juvenile idiopathic arthritis activity was observed in 31 (26.2%) patients, equally often in all subgroups of children. Index functional state did not show a significant decrease either in the whole group or in each of the arthritis subgroups. The overall indicator of quality of life in children with juvenile idiopathic arthritis was reduced in the whole group (71.2±1.4 and 72.9±1.4 per week and month). There was no significant difference between the quality of life indicators of boys and girls. at the same time, physical activity indicators were the lowest in the group with polyarticular juvenile idiopathic arthritis, regardless of gender and age of children, and especially low in children with polyarthritis in the first year of the disease. They also turned out to be worse in children with uveitis-associated subtypes of juvenile idiopathic arthritis with the disease from one to three years. The highest level of the physical component of quality of life was observed in children with oligoarthritis older than 14 years and in children under 8 years of age in the uveitis-associated subtypes of juvenile idiopathic arthritis group. There was no significant effect on the physical indicators of quality of life of the start treatment timing. (р≤0,05). Conclusions. A decrease in quality of life and its physical component is typical for children with different types of juvenile idiopathic arthriti (oligoarticular, polyarticular, and uveitis-associated subtypes of juvenile idiopathic arthritis). It has been established that children with polyarticular subtype of arthritis have the greatest decrease in quality of life and physical functioning.
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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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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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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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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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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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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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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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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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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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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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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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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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Sá-Nakanishi, Anacharis B., Jamil Soni-Neto, Lucas S. Moreira, Geferson A. Gonçalves, Francielli M. S. Silva, Lívia Bracht, Ciomar A. Bersani-Amado, Rosane M. Peralta, Adelar Bracht, and Jurandir F. Comar. "Anti-Inflammatory and Antioxidant Actions of Methyl Jasmonate Are Associated with Metabolic Modifications in the Liver of Arthritic Rats." Oxidative Medicine and Cellular Longevity 2018 (August 23, 2018): 1–16. http://dx.doi.org/10.1155/2018/2056250.
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Methyl jasmonate (MeJA) is a fatty acid-derived cyclopentanone which shares structural similarities with prostaglandins and has been under study as a promising anti-inflammatory agent. This study investigated the actions of MeJA on systemic inflammation and oxidative status in rats with adjuvant-induced arthritis, a model for rheumatoid arthritis. MeJA (75 to 300 mg·kg−1) was administrated orally during 18 days after arthritis induction with Freund’s adjuvant. Articular and systemic inflammation was greatly increased in arthritic rats, likewise the oxidative stress in plasma and liver. The hepatic glucokinase activity and glycolysis were increased in arthritic rats. MeJA decreased most inflammatory parameters and abolished the increased protein carbonylation in plasma and liver, diminished the increased hepatic ROS content, and restored the hepatic GSH/GSSG ratio in arthritic rats. However, the MeJA treatment decreased the hepatic glucokinase activity and glycolysis and stimulated mitochondrial ROS production in healthy and arthritic rats. Oxygen uptake was increased by MeJA only in livers from treated arthritic rats. This action may bear relation to the increased activity of mitochondrial NADP+-dependent enzymes to provide reducing equivalents for the glutathione cycle. These beneficial effects, however, are associated with a decreased glucose flux through the glycolysis in the liver of arthritic and healthy rats.
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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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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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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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Ibanez De Caceres, I., MA Villanua, L. Soto, AI Martin, and A. Lopez-Calderon. "IGF-I and IGF-I-binding proteins in rats with adjuvant-induced arthritis given recombinant human growth hormone." Journal of Endocrinology 165, no. 3 (June 1, 2000): 537–44. http://dx.doi.org/10.1677/joe.0.1650537.
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Adjuvant-induced arthritis in rats is associated with growth failure, hypermetabolism and accelerated protein breakdown. We have previously reported that adjuvant-induced arthritis in rats results in a decrease in body weight gain, pituitary GH mRNA, circulating GH and IGF-I together with an increase in serum IGF-binding proteins (IGFBPs). The aim of this study was to analyze the role of GH in the decrease in body weight and in the alterations in the IGF-I system observed in chronic inflammation. Male Wistar rats were injected with complete Freund's adjuvant and 16 days later arthritic rats were injected daily with recombinant human GH (rhGH) (3 IU/kg s.c.) for 8 days; control rats received 250 microl saline. Arthritis significantly decreased body weight gain and serum IGF-I. These decreases were not due to the reduced food intake, since in pair-fed rats they were not observed. Furthermore, administration of rhGH to arthritic rats increased body weight gain without modifying food intake. To further investigate the effect of GH administration, 14 days after adjuvant injection both control and arthritic rats were treated with 0, 1.5, 3 or 6 IU/kg of rhGH. GH treatment at the dose of 3 and 6 IU/kg significantly increased body weight gain in arthritic rats. GH administration, at the higher dose of 6 IU/kg, increased hepatic and serum concentrations of IGF-I in both control and arthritic rats. In control rats, rhGH at the three doses assayed increased circulating IGFBP-3. GH treatment in arthritic rats decreased IGFBP-1 and -2, and did not modify IGFBP-4. GH treatment at the dose of 3 IU/kg also decreased circulating IGFBP-3 in arthritic rats. These data suggest that GH treatment can ameliorate the catabolism observed in adjuvant-induced arthritis, an effect mediated, at least in part, by modifications in the circulating IGFBPs.
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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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Haleagrahara, Nagaraja, Dulanthi Tudawe, Srikumar Chakravarthi, and Ammu Kutty Radhakrishnan. "Amelioration of Collagen-Induced Arthritis in Female Dark Agouti Rats by Glucosamine Treatment." ISRN Pharmacology 2013 (February 14, 2013): 1–7. http://dx.doi.org/10.1155/2013/562905.
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The present study assessed the therapeutic efficacy of glucosamine hydrochloride against collagen-induced arthritis in female Dark Agouti rats (DA). Arthritis was induced by intradermaly injecting a collagen and complete Freund’s adjuvant suspension at multiple sites in the rat at a dose of 4 mg/kg of body weight and thereafter followed by two more boosters of the same dose, after the 1st week and 2nd week of primary immunization. After 21 days from the day of primary immunization, the arthritic group rats were given oral supplementation of glucosamine hydrochloride at a dose of 300 mg/kg of body weight until day 45. The arthritic group treated with glucosamine hydrochloride from day 21 to day 45 showed significant reduction in arthritic histopathological changes of the joints, reduction in paw thickness and also a significant decrease in C-reactive protein and TNF-alpha in the serum. Treatment with 300 mg/kg of glucosamine hydrochloride was able to reverse the arthritic changes, hence suggesting that glucosamine has a therapeutic effect against collagen-induced 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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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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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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Choi, Jun Young, Jin Soo Suh, and Dong Joo Lee. "Factors influencing medial sesamoid arthritis in patients with hallux valgus deformity." Foot & Ankle Orthopaedics 3, no. 3 (July 1, 2018): 2473011418S0019. http://dx.doi.org/10.1177/2473011418s00192.
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Category: Midfoot/Forefoot Introduction/Purpose: The importance of preoperative evaluation of the position and degree of arthritic changes of the medial sesamoid bone before hallux valgus correction is emerging. This is an observational study to evaluate the magnetic resonance imaging (MRI) findings of hallux valgus deformity, and assess the severity of and identify the factors that influence the arthritic changes in medial sesamoid-metatarsal (mSM) joints. Methods: We reviewed weight-bearing anteroposterior radiographs, forefoot axial radiographs and MR images of 514 feet of 405 patients who underwent hallux valgus correction. On MRI, the degrees of the arthritic changes in the first metatarsophalangeal (MTP) and mSM joints were categorized into 5 classes. Binary logistic regression analysis was performed to identify the factors affecting the arthritic changes. Results: The binary logistic regression analysis showed that advanced age, more lateralized position of medial sesamoid bone on forefoot axial radiograph, and higher MRI grade of arthritic change of the 1st MTP joint were significant factors contributing to medial sesamoid arthritis (P <0.001, 0.001. 0.006, respectively). Conclusion: Medial sesamoid arthritis can be assessed using MRI. The position of medial sesamoid bone on forefoot axial radiographs can strongly help predict the possibility of mSM joint arthritis.
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Guo, Chunqing, Fanlei Hu, Zhanguo Li, and Xiang-Yang Wang. "A potential pathogenic role of myeloid derived suppressor cells in autoimmune arthritis (IRC5P.457)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 125.6. http://dx.doi.org/10.4049/jimmunol.192.supp.125.6.
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Abstract Myeloid-derived suppressor cells (MDSCs) are a heterogeneous population of myeloid progenitor cells and immature myeloid cells. Although the role of MDSCs in tumor immune evasion during cancer progression has received much attention, its involvement in other inflammatory autoimmune diseases, such as rheumatoid arthritis (RA) remains largely unknown. We show that the levels of MDSCs are significantly elevated in RA patients and during the progression of collage-induced arthritis (CIA) in mice. While MDSCs in arthritic mice are phenotypically distinct from neutrophils or inflammatory monocytes, they display strong T-cell suppressive activity in vitro, resembling the functionality of tumor expanded MDSCs. Surprisingly, the expansion of MDSCs in lymphoid organs or inflamed joints positively correlate with the disease severity in arthritic mice and RA patients. Additionally, MDSCs from arthritic mice or RA patients efficiently promote the differentiation of naïve CD4+ T cell precursors into T-helper 17 (Th17) cells. Furthermore, pharmacologic elimination or antibody depletion of MDSCs attenuates a Th17 response in arthritic mice, which concomitantly reduces articular cartilage damage and ameliorates the established disease. Our results suggest that an excessive accumulation of MDSCs may exacerbate autoimmune arthritic disease by promoting inflammatory Th17 cells. MDSCs may be exploited as a potential cellular target of intervention in autoimmune 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.
Full textAbstract:
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.
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Li, Ting, Kangsheng Liao, Yuxin Zhuang, Jianlin Wu, and Juan Liu. "C15 is actionable drug target for anti-arthritis via activation Nrf2 signaling." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 133.12. http://dx.doi.org/10.4049/jimmunol.202.supp.133.12.
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Abstract SNM is a purified compound isolated from Chinese Medicinal plant. In the current study, we found that SNM not only ameliorated the progression of collagen induced arthritis (CIA), but protected joints from destruction in mice, indicating that SNM probably restricted the local inflammation of arthritic joints. As synovium in the joints is the major target tissue of rheumatoid arthritis, the synovium fibroblasts derived from RA patients (RASFs) were employed to validate the anti-arthritic effect and explore underlying mechanism of SNM. The results demonstrated that SNM significantly inhibited IL-6 and IL-33 secretion, COX-2 expression and ROS production in RASFs. Mass spectrometry results demonstrated that cysteine 26 (C26) and lysine 873 (K873) of C15 are a direct target of SNM. Underlying mechanistic study showed that knockdown C15 resulted in the accumulation and phosphorylation of p62 and aggregation of Nrf2 and HO-1 in cytoplasma of RASFs. Consistently, SNM activated p62/Nrf2 signaling in RASFs via covalently binding at C26 and K873 of C15. Furthermore, the collagen antibody-induced arthritis (CAIA) model was established in Nrf2−/− mice to verify the role of Nrf2 in the anti-arthritic effect of SNM, and the results explored that Nrf2−/− mice are resistant to the anti-arthritic effect of SNM. Our findings explored that C15 is an actionable drug target for anti-arthritis via activation Nrf2 signaling.
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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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Spargo, L. D., J. S. Hawkes, L. G. Cleland, and G. Mayrhofer. "Recruitment of lymphoblasts derived from peripheral and intestinal lymph to synovium and other tissues in normal rats and rats with adjuvant arthritis." Journal of Immunology 157, no. 11 (December 1, 1996): 5198–207. http://dx.doi.org/10.4049/jimmunol.157.11.5198.
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Abstract Recruitment of [125I]iododeoxyuridine-labeled syngeneic lymphoblasts from thoracic duct (TD) lymph into periarticular tissues has been examined after intravenous administration to normal rats and to rats with adjuvant-induced arthritis. Uptake of label was observed in the inflamed paws of arthritic rats and cells were located in synovium and periarticular bone marrow by autoradiography. Uptake was greater with lymphoblasts from donors in the late prodromal phase of adjuvant-induced arthritis (arthritic donors) than from normal donors. With arthritic donors, recruitment of lymphoblasts from TD lymph was greater than from mesenteric duct lymph, suggesting that most of the joint-seeking lymphoblasts in arthritic rats arose in peripheral lymphoid tissues. Lymphoblasts from arthritic donors were also detected in the synovium of paws from normal rats. Recovery of lymphoblasts was monitored in other tissues; this revealed, in arthritic recipients, competition among extra-articular sites of inflammation (adjuvant injection site, draining lymph nodes, and lymph nodes draining affected joints), the lungs, and the inflamed synovium for recruitment of lymphoblasts from arthritic donors. In contrast, while some lymphoblasts from normal donors were recruited to inflamed joints, the small intestine was the main site of recruitment. The results reflect the known propensity of T lymphoblasts generated in peripheral lymphoid tissues to enter inflamed tissues. However, some mesenteric duct lymphoblasts also entered inflamed synovium. The observed pattern of recruitment of lymphoblasts to synovium is pertinent to the pathogenesis of arthritis, the potential roles of arthritogenic and "bystander" lymphocytes and the known links between the joints and inflammation in the intestine.
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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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Chang, Jia-Ming, Chun-Ming Cheng, Le-Mei Hung, Yuh-Shan Chung, and Rey-Yuh Wu. "Potential Use ofPlectranthus amboinicusin the Treatment of Rheumatoid Arthritis." Evidence-Based Complementary and Alternative Medicine 7, no. 1 (2010): 115–20. http://dx.doi.org/10.1093/ecam/nem168.
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Plectranthus amboinicus(P. amboinicus) is a folk herb that is used to treat inflammatory diseases or swelling symptoms in Taiwan. We investigated therapeutic efficacy ofP. amboinicusin treating Rheumatoid Arthritis (RA) using collagen-induced arthritis animal model. Arthritis was induced in Lewis rats by immunization with bovine type II collagen. Serum anti-collagen IgG, IgM and C-reactive protein (CRP) were analyzed. To understand the inflammation condition of treated animals, production of TNF-α, IL-6 and IL-1β from peritoneal exudates cells (PEC) were also analyzed.P. amboinicussignificantly inhibited the footpad swelling and arthritic symptoms in collagen-induced arthritic rats, while the serum anti-collagen IgM and CRP levels were consistently decreased. The production of pro-inflammatory cytokines TNF-α, IL-6 and IL-1β were also decreased in the high dosage ofP. amboinicusgroup. Here, we demonstrate the potential anti-arthritic effect ofP. amboinicusfor treating RA, which might confer its anti-rheumatic activity. This differs the pharmacological action mode of indomethacin.
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Bista, Krishna Bahadur, PP Lamichhane, SM Regmi, A. Naglla, and S. Shrestha. "Normal or Arthritic: Is 25-hydroxy Vitamin D status significant?" Journal of Gandaki Medical College-Nepal 10, no. 1 (August 1, 2017): 21–24. http://dx.doi.org/10.3126/jgmcn.v10i1.17908.
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Background: Vitamin D is required for proper skeletal development and function. However, the status of vitamin D in healthy subjects and those suffering from arthritis in Nepal is largely unknown.Objective: This study measured vitamin D level in healthy and arthritic individuals of Western Nepal.Methods: Vitamin D level in healthy and arthritic subjects were measured by using LIASION 25-hydroxy Vitamin D assay, a direct competitive chemiluminescence immunoassay (CLIA).Results: Our result suggested that most of the subjects, irrespective of age and disease condition, have subnormal/normal level of vitamin D (≥16ng/mL). Also, the data suggested that serum vitamin D level is significantly higher in males than in females. Moreover, the vitamin D level is higher in healthy individuals when compared with those suffering from arthritis. However, vitamin D level in normal subjects and arthritic patients could not be correlated.Conclusion: Vitamin D level is higher in normal subjects compared to arthritic individuals. However, the level could not be correlated suggesting need of a pilot study to determine vitamin D level and its association with arthritis in Nepalese.Journal of Gandaki Medical College Vol. 10, No. 1, 2017, Page: 21-24
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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.
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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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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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Suseela, Prema, and Chitra Krishnan. "Anti-Arthritic Potential of Ethyl Acetate Extract of Stereospermum colais in Animal Model." Journal of Evolution of Medical and Dental Sciences 10, no. 14 (April 5, 2021): 991–98. http://dx.doi.org/10.14260/jemds/2021/213.
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BACKGROUND Stereospermum colais also known as yellow snake tree is widely utilised to alleviate rheumatic pain and inflammation in the conventional medicinal system. Lapachol has been reported to be anti-inflammatory by inhibiting the production of nitric oxide (NO) and tumour necrosis factor (TNF)-alpha by means of modulating the metabolism of arachidonic acid, activation of NF-aB, suppression of nitric oxide synthase (iNOS) expression and expression of cyclooxygenase-2 (COX-2). It has also been analysed for anticancer and antioxidant activity, renal disorders, endometriosis and cardiac dysfunction. The present study investigates the anti– arthritic activity of the ethyl acetate extracts of Stereospermum colais. METHODS The fruit rind of Garcinia indica was used to prepare extract and was quantified using liquid chromatography–mass spectrometry (LC-MS) / MS. Ethyl acetate extract showed increased content of the phytochemical constituent necessary for the treatment of arthritic pain. So, the ethyl acetate extract of bark of S. colais was evaluated for anti-arthritic activity by complete Freund's adjuvant (CFA). Arthritis index, body weight changes, and the biochemical analysis parameters were measured. Histopathological evaluation along with TNF-alpha and interleukin (IL)-6 assays were also studied. RESULTS The ethyl acetate extract showed significant reduction in arthritis index (P < 0.01), paw swelling (P < 0.01) and arthritic score (P < 0.01), thereby demonstrating antiinflammatory potential. A good improvement in the biochemical parameters in extract treated animals indicates good protection against the inflammation. CONCLUSIONS The results show that Stereospermum colais can be used as a potential anti arthritic drug. KEY WORDS Rheumatoid Arthritis, Complete Freund’s Adjuvant, Stereospermum colais, Ethyl Acetate, Anti-Arthritis, Meloxicam
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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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Belal, Amany, Rehab Mahmoud, Mohamed Taha, Fatma Mohamed Halfaya, Ahmed Hassaballa, Esraa Salah Elbanna, Esraa Khaled, et al. "Therapeutic Potential of Zeolites/Vitamin B12 Nanocomposite on Complete Freund’s Adjuvant-Induced Arthritis as a Bone Disorder: In Vivo Study and Bio-Molecular Investigations." Pharmaceuticals 16, no. 2 (February 13, 2023): 285. http://dx.doi.org/10.3390/ph16020285.
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Rheumatoid arthritis (RA) is a long-term autoimmune disease. As nanotechnology has advanced, a growing number of nanodrugs have been used in the treatment of RA due to their unique physical and chemical properties. The purpose of this study was to assess the therapeutic potential of a novel zeolite/vitamin B12 nanocomposite (Nano ZT/Vit B12) formulation in complete Freund’s adjuvant (CFA)-induced arthritis. The newly synthesized Nano ZT/Vit B12 was fully characterized using various techniques such as XRD, FT-IR, BET analysis, HERTEM, SEM, practical size, zeta potential, XRF, and EDX. The anti-arthritic, anti-inflammatory, and antioxidant activities as well as the immunomodulation effect of Nano ZT/Vit B12 on the CFA rat model of arthritis were examined. Histopathologic ankle joint injuries caused by CFA intrapedal injection included synovium hyperplasia, inflammatory cell infiltration, and extensive cartilage deterioration. The arthritic rats’ Nano ZT/Vit B12 supplementation significantly improved these effects. Furthermore, in arthritic rats, Nano ZT/Vit B12 significantly reduced serum levels of RF and CRP, as well as the levels of IL-1β, TNF-α, IL-17, and ADAMTS-5, while increasing IL-4 and TIMP-3 levels. Nano-ZT/Vit B12 significantly declined the LPO level and increased antioxidant activities, such as GSH content and GST activity, in the arthritic rats. In arthritic rats, Nano ZT/Vit B12 also reduced TGF-β mRNA gene expression and MMP-13 protein levels. Collectively, Nano ZT/Vit B12 seems to have anti-arthritic, anti-inflammatory, and antioxidant properties, making it a promising option for RA in the future.
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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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Fan, Yi, Cheng Zhang, Guotao Zheng, Shuai Wu, Yujie Wang, and Jinsong Bian. "Ameliorative and anti-arthritic potential of arjunolic acid against complete Freund’s adjuvant-induced arthritis in rats." Tropical Journal of Pharmaceutical Research 19, no. 9 (November 24, 2020): 1933–39. http://dx.doi.org/10.4314/tjpr.v19i9.19.
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Purpose: To determine the anti-arthritic effect of arjunolic acid against complete Freund’s adjuvant (CFA)-induced arthritis in rats.Methods: Arthritis was induced in male Sprague Dawley rats by intradermal injection of 0.1 mL of CFA at the right footpad. Upon induction of osteoarthritis, arjunolic acid was administered via oral gavage at doses of 40 and 80 mg/kg once daily for 25 successive days. Indomethacin was used as reference drug at a dose of 3 mg/kg via gavage twice weekly for 25 days. Changes in paw swelling, serum hematology, antioxidant enzymes, serum inflammatory mediators, and histopathology were determined using standard procedures.Results: Paw swelling and weight loss in CFA-induced arthritic rats were significantly reversed (p < 0.01) by arjunolic acid. Malondialdehyde (MDA) levels, spleen index and thymus index were significantly reduced in CFA-induced arthritic rats (p < 0.01). Moreover, arjunolic significantly increased superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities, while downregulating the expressions of TNF-α, IL-1β and IL-6 in serum (p < 0.01). The hematological and histopathological changes due to CFA-induced arthritis were ameliorated by arjunolic acid.Conclusion: The results obtained in this study indicate that arjunolic acid may possess therapeutic potentials for the management of arthritis.
Keywords: Arjunolic acid, Triterpenoid; Oxidative stress, osteoarthritis, Inflammation