Journal articles: 'Adjuvant arthritis'

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Conforti, A., S. Lussignoli, S. Bertani, R. Ortolani, G. Verlato, and P. Bellavite. "Intraperitoneal Administration of Adjuvant Inhibits the Development of Adjuvant Arthritis in Rats." International Journal of Immunopathology and Pharmacology 8, no. 2 (May 1995): 113–21. http://dx.doi.org/10.1177/039463209500800206.

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In recent years, considerable efforts have been made to develop effective therapy for autoimmune diseases by specific suppression of the autoreactive immune process without affecting the remainder of the immune system. In our study we evaluated the protective effects and therapeutic potential of Mycobacterium butyricum (Mb), the causative antigen inducing adjuvant arthritis (AA), an experimental model of autoimmune disease in the rat. The antigen was administered to rats by a different route and at concentrations 10 and 100 times lower than the inducing one. Arthritis was induced by injection of 0.6 mg of Mb in paraffin oil into the hindpaw, and the severity of disease was assessed by measurement of contralateral paw swelling every three days and primary and secondary lesions were scored on an arbitrary scale after 14, 21, and 28 days. Animals were assigned to different groups and treated intraperitoneally with different doses and schedules of Mb. The administration of 60 μg of Mb every two days, starting 6 days before arthritogenic injection until the second day after, led to a significant inhibition of the arthritic process (p< 0.001 of the arthritic index). Treatment of animals with 60 μg of Mb every two days, from day 2 to day 21 after arthritis induction caused almost total suppression of lesions. However, in both treatment schedules, animals showed important signs of peritoneal inflammation. The administration of single injection of 60 or 6 μg of Mb 10 days after arthritis induction led to an inhibition of arthritic index reaching the maximum percentage on day 14 (26% and 24% with 60 and 6 μg respectively) and was able to delay the development of oedema foot volume, without signs of local inflammation. These results confirm the ability to modulate the autoimmune process even when the immunological response is far advanced, suggesting new strategies in the therapy of human autoimmune diseases.

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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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Davis, RH, KY Rosenthal, LR Cesario, and GR Rouw. "Vitamin C influence on localized adjuvant arthritis." Journal of the American Podiatric Medical Association 80, no. 8 (August 1, 1990): 414–18. http://dx.doi.org/10.7547/87507315-80-8-414.

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This work attempts to determine the influence of vitamin C on locally induced inflammation and arthritis in rat paws, as measured by rat paw swelling, polymorphonuclear leukocyte infiltration, pain, and surface skin temperature. Daily subcutaneous administration of 150 mg/kg of vitamin C over 20 days reduced arthritic swelling, increased pain tolerance, and decreased polymorphonuclear leukocyte infiltration, with no significant change in surface temperature. Vitamin C may provide podiatrists with a supplemental or alternative treatment for patients with rheumatoid arthritis.

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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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Chen, Xi, Cheng Yi Zhang, and Hao Gang Xue. "Effect of Arthrigia on Adjuvant Arthritis Rats’ IL-12." Applied Mechanics and Materials 140 (November 2011): 43–47. http://dx.doi.org/10.4028/www.scientific.net/amm.140.43.

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Rheumatoid Arthritis （RA） is a systemic chronic autoimmune disease. To study the therapeutic mechanism of effects of Skullcap Brightviolet （SB），glucosamine/chondroitin （GC），and the combination of them (named Arthrigia) on RA. With the adjuvant arthritis (AA) rat models, we observed the protective effects of oral SB, GC and Arthrigia in different concentrations on AA in rats. We further examined the immunological mechanism of the combination of them by testing the rats’ secretion of IL-12. The results showed that Arthrigia inhibited the production and secretion of IL-12 factors in some extent, and its effects are more potent the single SB or GC. The present study provides the experimental evidences for Arthrigia for its further development, clinical prevention and treatment of RA.

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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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WARD, P. A. "Neutrophils and adjuvant arthritis." Clinical & Experimental Immunology 107, no. 2 (February 1997): 225–26. http://dx.doi.org/10.1111/j.1365-2249.1997.00276.x.

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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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Al-Okbi, S. Y., and D. A. Mohamed. "Preparation and evaluation of functional foods in adjuvant arthritis." Grasas y Aceites 63, no. 4 (October 25, 2012): 394–402. http://dx.doi.org/10.3989/gya.130811.

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Zhang, Maoquan, Baolong Liu, and Zonghui Ji. "Effect of Wu-Wei-Gui-Shao decoction on complete Freund's adjuvant-induced arthritis rats." Tropical Journal of Pharmaceutical Research 19, no. 9 (November 24, 2020): 1977–83. http://dx.doi.org/10.4314/tjpr.v19i9.25.

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Purpose: To investigate the anti-rheumatic potential of Wu-Wei-Gui-Shao decoction (WGD) and its possible mechanism of action. Methods: Adjuvant arthritis (AA) rats were established using complete Freund's adjuvant. The rats were then given different doses of WGD (100, 200, and 400 mg/kg, for 28 days). The anti-arthritic effects of WGD were evaluated. Furthermore, the in vitro anti-arthritic effects of WGD and its related mechanisms were also determined in MH7A cells. Results: WGD (100 - 400 mg/kg) exhibited significant anti-rheumatic properties after 28 days of treatment, inhibiting paw edema in AA rats, reducing arthritis score and thymus and spleen index, and inhibiting the tumor necrosis factor (TNF)-α and the interleukin (IL)-6. In addition, the results of in vitro cell experiments also confirmed that WGD reduced the release of cytokines, as well as mRNA levels of matrix metalloproteinase (MMP) -2, -3, and -9. Conclusion: These findings suggest that WGD can be further developed as a traditional Chinese medicine to treat rheumatic arthritis. Keywords: Wu-Wei-Gui-Shao decoction, Complete Freund's adjuvant, Arthritis, Molecular mechanism, Traditional Chinese Medicine

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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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Baroroh, Hanif Nasiatul, Esti Dyah Utami, and Anisyah Achmad. "Psidium guajava leaves decrease arthritic symptoms in adjuvant-induced arthritic rats." Universa Medicina 34, no. 3 (April 27, 2016): 197. http://dx.doi.org/10.18051/univmed.2015.v34.197-204.

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BACKGROUND Guava is an herbal with proven antioxidant and anti-inflammatory properties. The aim of this study was to investigate the anti-arthritic activity of the ethanol extract of Psidium gujava leaves (EEPG) against complete Freund’s adjuvant (CFA) induced arthritis in rats. METHODS An experimental study was conducted on 40 male Wistar Sprague Dawley rats, which were divided into 5 groups. Each group was induced with 0.2 mL CFA (1 mg/mL) on day 1 and 0.1 CFA mL booster injection on day 5. Group I served as an arthritic control, group II received dexamethasone (6.75 mg.kg-1 orally), group III, IV and V received EEPG at oral doses of 250, 500, and 750 mg/kg BW, respectively, on days 14 to 28. Anti-arthritic activity was observed from the arthritis score, the paw circumference was measured on days 0, 1, 4, 8, 12, 16, 20, 24, and 28, the mobility score was determined on days 12 and 28, and the histolopathology of the knee joint was examined on day 29. RESULTS Ethanol extract of Psidium guajava leaves significantly suppressed the swelling of the paws in chronic phase based on increasing of edema (%), while starting on day 20. EEPG at 250 mg/kg was most effective in significantly reducing arthritis scores (p<0.05). Histopathological examination showed repair of the knee joint synovial membrane and cartilage. CONCLUSIONS Psidium guajava leaf extract is effective in decreasing the inflammatory response and arthritic symptoms in rats with adjuvant-induced arthritis. Psidium guajava leaves can be developed into an alternative anti-arthritis treatment.

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Kang, Seong Soo, Sok Cheon Pak, and Seok Hwa Choi. "The Effect of Whole Bee Venom on Arthritis." American Journal of Chinese Medicine 30, no. 01 (January 2002): 73–80. http://dx.doi.org/10.1142/s0192415x02000089.

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This study was performed to assess the clincotherapeutic effect of whole venom of honeybee (Apis mellifera) in adjuvant-induced arthritic rat. Ninety Sprague-Dawley male rats were injected with complete Freund's adjuvant (CFA). Adjuvant arthritis was produced by a single subcutaneous injection of 1 mg Mycobacterium butyricum suspended in 0.1 ml paraffin oil into the right hind paw. Righting reflex was uniformly lost and considered to be the point of arthritis development on day 14 after CFA injection. The experiments were divided into three groups. When arthritis was developed in the rat, tested groups were administered with prednisolone (10 mg/kg, p.o.) or honeybee venom (one bee, s.c.) every other day for another 14 days. Control group was injected with 0.1 ml of physiological saline solution subcutaneously. Clinical and hematological values with histopathological findings were observed during the drug administration. In treatment groups, the development of inflammatory edema and polyarthritis was suppressed. No significant differences of hind paw edema volume and lameness score between prednisolone and honeybee venom groups were observed during treatment. White blood cell counts of control group showed leucocytosis that was significantly different from the two treatment groups (p < 0.01). Erosions of articular cartilage and inflammatory cell infiltrations into interphalangeal joint were effectively suppressed in treated groups. In conclusion, whole honeybee venom was found to suppress arthritic inflammation in the rat. This may be an alternative treatment of arthritic agony in humans.

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Alamgeer, Umme Habiba Hasan, Ambreen Malik Uttra, and Shahid Rasool. "Evaluation of in vitro and in vivo anti-arthritic potential of Berberis calliobotrys." Bangladesh Journal of Pharmacology 10, no. 4 (September 30, 2015): 807. http://dx.doi.org/10.3329/bjp.v10i4.23779.

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The present study was commenced to evaluate the anti-arthritic effect of 70% methanol extract and n-butanol and aqueous fractions of Berberis calliobotrys using both in vitro and in vivo arthritis models. Extract and fractions were investigated in vitro for inhibition of protein (bovine serum and egg albumin) denaturation and human red blood cell membrane stabilization. In vivo anti-arthritic activity of extract and fractions at 50, 100 and 200 mg/kg was assessed using turpentine oil and formaldehyde-induced arthritis, while, 200 mg/kg dose was evaluated against complete Freund’s adjuvant-induced arthritis. B. calliobotrys produced significant (p<0.001) dose dependent inhibition of protein denaturation and human red blood cell membrane stabilization. In turpentine oil, formaldehyde and complete Freund’s adjuvant-induced arthritis models, B. calliobotrys significantly (p<0.001) reduced joint and paw swelling. B. calliobotrys markedly improved body weight, hematology profile, radiological and histopathological parameters in complete Freund’s adjuvant model. It could be concluded that B. calliobotrys holds anti-arthritic potential, supporting its traditional use in treatment of rheumatoid arthritis.

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Martín, A. I., E. Castillero, M. Granado, M. López-Menduiña, M. A. Villanúa, and A. López-Calderón. "Adipose tissue loss in adjuvant arthritis is associated with a decrease in lipogenesis, but not with an increase in lipolysis." Journal of Endocrinology 197, no. 1 (January 8, 2008): 111–19. http://dx.doi.org/10.1677/joe-07-0491.

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Adjuvant-induced arthritis is a model of rheumatoid arthritis that induces cachexia. In other cachectic situations, there is an increase in lipolysis resulting in a loss of adipose tissue mass. The aim of this work was to analyse the effect of chronic arthritis, induced by adjuvant injection, on white adipose tissue (WAT). For this purpose, rats were killed 10 days after adjuvant injection, when the first external symptoms appeared, on days 15 and 22 when the external signs of the illness reach their severest level. As arthritis decreases food intake, a pair-fed group was also included. Serum concentrations of insulin, leptin, adiponectin, glycerol and nitrites, as well as gene expression of leptin, adiponectin, hormone-sensitive lipase (HSL), fatty acid synthase (FAS), tumour necrosis factor α and zinc-α2-glycoprotein (ZAG) were determined. Arthritis decreased food intake between days 5 and 16, but not during the last 5 days of the experiment. There was a marked decrease in relative adipose tissue weight and in serum leptin and adiponectin as well as in their gene expression in WAT in arthritic rats. Arthritis decreased the gene expression of FAS in the WAT. However, none of these effects was found in pair-fed rats. Arthritis did not increase lipolysis, since arthritic rats have lower serum concentrations of glycerol, HSL mRNA in WAT, as well as liver ZAG mRNA than the pair-fed or control rats. These data suggest that in chronic arthritis the decrease in white adipose mass is secondary to a reduced adipose lipogenesis, and this effect is not mainly due to the decrease in food intake.

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Ibanez De Caceres, I., JM Holly, T. Priego, AI Martin, A. Lopez-Calderon, and MA Villanua. "Arthritis-induced increase in serum levels of IGF-binding protein-3 in rats is secondary to the decrease in its proteolytic activity." Journal of Endocrinology 173, no. 2 (May 1, 2002): 357–64. http://dx.doi.org/10.1677/joe.0.1730357.

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Adjuvant-induced arthritis is a chronic inflammatory illness that induces a catabolic state, with a decrease in pituitary GH and hepatic IGF-I synthesis. We have previously observed an increase in serum IGF-binding protein-3 (IGFBP-3) in arthritic rats, and found that GH administration prevents the increase in circulating IGFBP-3 in arthritic rats. The aim of this work was therefore to study IGFBP-3 synthesis in the liver as well as its proteolysis in serum as the two possible causes of the increased circulating IGFBP-3 in arthritic rats. The effect of recombinant human GH (rhGH) administration was also analysed. Adult male Wistar rats were injected with complete Freund's adjuvant or vehicle, and 14 days later they were injected s.c. daily until day 22 after adjuvant injection with rhGH (3 IU/kg) or saline. Three hours after the last GH injection, all rats were killed by decapitation. Arthritis increased serum IGFBP-3 levels (P<0.01). The increase in serum IGFBP-3 levels in arthritic rats seems to be due to decreased proteolysis (P<0.01) rather than to an increased synthesis, since liver IGFBP-3 mRNA content was not modified by arthritis. GH administration to control rats resulted in an increase in both hepatic IGFBP-3 mRNA content and in serum IGFBP-3 levels in spite of the increase in IGFBP-3 proteolysis in serum. In arthritic rats, GH treatment did not modify liver IGFBP-3 synthesis, but it increased serum proteolysis of IGFBP-3, leading to a serum concentration of IGFBP-3 similar to that of control rats. Furthermore, there was a negative correlation between circulating IGFBP-3 and its proteolytic activity in the serum of adjuvant-induced arthritic rats. These data suggest that in chronic arthritis the increase in IGFBP-3 serum concentration is secondary to a decrease in proteolytic activity, rather than to an increase in hepatic IGFBP-3 gene expression.

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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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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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Nasuti, Cinzia, Donatella Fedeli, Laura Bordoni, Marco Piangerelli, Maurizio Servili, Roberto Selvaggini, and Rosita Gabbianelli. "Anti-Inflammatory, Anti-Arthritic and Anti-Nociceptive Activities of Nigella sativa Oil in a Rat Model of Arthritis." Antioxidants 8, no. 9 (August 25, 2019): 342. http://dx.doi.org/10.3390/antiox8090342.

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This study investigated the preventive efficacy of the crude oil extracted from Nigella sativa seeds in a rat model of arthritis induced by using complete Freund’s adjuvant (CFA). Nigella sativa oil at 1.82 mL/kg or 0.91 mL/kg (corresponding to 1596 and 798 mg/kg, respectively) was orally administered for 25 days from the day of immunization. One immunized group was treated orally with indomethacin (3 mg/kg) as a reference drug. Body weight growth rate, paw swelling, arthritis score, mechanical allodynia, locomotor activity and anxiety-like behavior were observed, and the levels of Interleukin 6 (IL-6), C-reactive protein, albumin and total cholesterol in plasma were measured on days 15 and 25. Nigella sativa oil showed anti-inflammatory, anti-arthritic and anti-nociceptive activities that were significant as compared to untreated arthritic rats but less than indomethacin. These results indicated that Nigella sativa oil significantly attenuated adjuvant-arthritis in rats and the higher dose (1.82 mL/kg) prevented the development of arthritis with an inhibition of 56%.

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Dong, Mei, Dongsheng Yu, Naif Abdullah Al-Dhabi, and Veeramuthu Duraipandiyan. "The Impacts ofChrysanthemum indicumExtract on Oxidative Stress and Inflammatory Responses in Adjuvant-Induced Arthritic Rats." Evidence-Based Complementary and Alternative Medicine 2017 (2017): 1–7. http://dx.doi.org/10.1155/2017/3285394.

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Chrysanthemum indicumhas been used as a therapeutic agent against inflammation, hypertension, and respiratory conditions for many years. This research’s aim has been to examine the antioxidant impacts thatChrysanthemum indicumextract (CIE) has on the oxidative stress and inflammatory responses in adjuvant-induced arthritic (AA) rats. 40 rats were categorised into 4 groups according to a completely randomized approach: Group I involved normal control rats (CTRL) that received a basal diet; Group II involved arthritic control rats (CTRL-AA) that received the same diet; Group III involved rats that received a basal diet and 30 mg/kg CIE; and Group IV involved arthritic rats with the same diet as Group III rats (CIE-AA). After injection with complete Freund’s adjuvant, body weight, arthritis score, and the serum levels of TNF-α, IL-1β, IL-6, myeloperoxidase (MPO), malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH-PX) were assessed. The results demonstrated that CIE delayed the onset time of arthritis and decreased the clinical arthritis severity score (P<0.05). Observations of CIE-AA and CTRL-AA rats demonstrated that CIE alleviates oxidative stress and inflammatory responses in CIE-AA group. In conclusion, CIE alleviated oxidative stress and inflammatory responses, thereby highlighting its potential use as a candidate for clinical treatments of 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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Lee, Jae Yeong, Joong-Hyun Kim, Seong Soo Kang, Chun Sik Bae, and Seok Hwa Choi. "The Effects of α-Viniferin on Adjuvant-Induced Arthritis in Rats." American Journal of Chinese Medicine 32, no. 04 (January 2004): 521–30. http://dx.doi.org/10.1142/s0192415x04002168.

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This study was performed to assess the efficacy of α-viniferin (Carex humilis Leyss) on adjuvant-induced arthritis in rats. Adjuvant arthritis was induced by a single subcutaneous injection of 0.1 ml complete Freund's adjuvant (CFA) containing 7.5 mg Mycobacterium butyricum suspended in 1 ml sterile paraffin oil into the right hind paw. Forty female Sprague-Dawley rats were injected. Righting reflex was uniformly lost and considered to be the initial point of arthritis development on day 7 after CFA injection. Rats were divided into four groups, and upon development of arthritis, tested groups were orally administered 3 or 10 mg/kg α-viniferin or 10 mg/kg ketoprofen every day for 14 days. The control group was orally administered 2 ml of physiological saline solution. Bone mineral density (BMD), radiological changes and edematous volumes were measured for 35 days. α-viniferin suppressed the development of inflammatory edema, and inhibited the bone destruction, noted with a decrease in BMD ( p <0.05). Hind paw edema volume, BMD and radiological changes did not differ significantly in the ketoprofen and α-viniferin groups during the entire study period. In conclusion, α-viniferin suppressed arthritic inflammation and bony change in rats.

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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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Sykora, Tomas, Pavel Babal, Kristina Mikus-Kuracinova, Frantisek Drafi, Silvester Ponist, Monika Dvorakova, Pavol Janega, and Katarina Bauerova. "Hyperbilirubinemia Maintained by Chronic Supplementation of Unconjugated Bilirubin Improves the Clinical Course of Experimental Autoimmune Arthritis." International Journal of Molecular Sciences 22, no. 16 (August 12, 2021): 8662. http://dx.doi.org/10.3390/ijms22168662.

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Rheumatoid arthritis (RA) is a chronic multisystem disease, therapy of which remains a challenge for basic research. The present work examined the effect of unconjugated bilirubin (UCB) administration in adjuvant-induced arthritis (AIA)—an experimental model, in which oxidative stress (OS), inflammation and inadequate immune response are often similar to RA. Male Lewis rats were randomized into groups: CO—control, AIA—untreated adjuvant-induced arthritis, AIA-BIL—adjuvant-induced arthritis administrated UCB, CO-BIL—control with administrated UCB. UCB was administered intraperitoneally 200 mg/kg of body weight daily from 14th day of the experiment, when clinical signs of the disease are fully manifested, to 28th day, the end of the experiment. AIA was induced by a single intradermal immunization at the base of the tail with suspension of Mycobacterium butyricum in incomplete Freund’s adjuvant. Clinical, hematologic, biochemical and histologic examinations were performed. UCB administration to animals with AIA lead to a significant decrease in hind paws volume, plasma levels of C-reactive protein (CRP) and ceruloplasmin, drop of leukocytes, lymphocytes, erythrocytes, hemoglobin and an increase in platelet count. UCB administration caused significantly lowered oxidative damage to DNA in arthritic animals, whereas in healthy controls it induced considerable oxidative damage to DNA. UCB administration also induced atrophy of the spleen and thymus in AIA and CO animals comparing to untreated animals. Histological signs of joint damage assessed by neutrophils infiltration and deposition of fibrin were significantly reduced by UCB administration. The effects of exogenously administered UCB to the animals with adjuvant-induced arthritis might be identified as therapeutic, in contrast to the effects of UCB administration in healthy animals rather classified as toxic.

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Xiaoming, Donghui Guo, Jianyong Zhao, Xing, Hengjun Wang, Shiqiang, Yunchao Zhao, and Xinlong. "Fisetin Attenuates Cartilage Destruction in Adjuvant-Induced Arthritis by Modulating Cartilage Cytokine Expression Correlated with Oxidative Status in the Early Phase in Experimental Animals." Folia Biologica 67, no. 4 (December 31, 2019): 177–89. http://dx.doi.org/10.3409/fb_67-4.18.

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The present study was designed to evaluate the effect of Fisetin on the progression of adjuvant-induced arthritis in rats and explore the mechanisms underlying fisetin mediated immunomodulation. Adjuvant-induced arthritis (AIA) was induced by a single subcutaneous injection of Freund's complete adjuvant (FCA). AIA rats were treated with Fisetin daily via oral gavage, for a period of 28 days. Paw swelling changes were assessed and histopathological and radiographic analysis was conducted to evaluate the antiarthritic effect. Lipid peroxidation and antioxidant enzyme activities in the joint tissue homogenate were performed to observe the modulation of the antioxidant status along the expression of different pro-inflammatory cartilage cytokines, such as TNF-á and IL-6. Fisetin promotes both the antiarthritic and the antioxidant effect, as well as the suppression of lipid peroxidation. Fisetin significantly inhibited the development phase of arthritis, as supported by histopathological and radiographical observations, and reduced overexpression of cartilage cytokines. Fisetin not only suppressed the arthritic progression and tissue destruction, but it also demonstrated a pronounced anti-inflammatory and immunomodulatory action against the immunosuppressive properties of AIA and provided a superior effect against inflammation. Furthermore, fisetin therapy restored the BMD loss and acts as a potent antioxidant and immunomodulator, suggesting that oral administration can suppress arthritic progression in rats.

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Mizukawa, Hiromi, Kazuo Yoshida, Akie Honmura, Yasuhiko Uchiyama, Hidehiko Kaku, Shigekatsu Nakajima, and Eiichi Haruki. "The Effect of Orengedokuto on Experimentally-inflamed Rats." American Journal of Chinese Medicine 21, no. 01 (January 1993): 71–78. http://dx.doi.org/10.1142/s0192415x93000091.

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The inhibitory effect of Orenge dokuto on lipid peroxide and sialidase was investigated using rats affected with carrageenin cotton pellet-induced granuloma and adjuvant arthritis. As a result, in the case of rats with carrageenin cotton pellet-induced granuloma, a significant inhibitory effect on granuloma formation was observed in the Orengedokuto treated rats (150 mg/kg/day) which showed a decrease in serum lipid peroxide ( p <0.001) and an increase in acid soluble glycoprotein ( p <0.001). In the case of adjuvant-induced arthritic rats, however, the condition of the arthritis was not improved at all, and was even aggravated in spite of the decrease in serum lipid peroxide.

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Kim, Jae-Hyo, Hee-Kee Kim, Yong-Il Park, In-Churl Sohn, Dong-Ok Choi, Min-Sun Kim, and Byung-Rim Park. "Moxibustion at ST36 Alleviates Pain in Complete Freund's Adjuvant-Induced Arthritic Rats." American Journal of Chinese Medicine 34, no. 01 (January 2006): 57–67. http://dx.doi.org/10.1142/s0192415x06003631.

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This study was to investigate the antinociceptive effects of moxibustion in a complete Freund's adjuvant (CFA)-induced arthritic rat model, and the effects of moxibustion on immunohistochemical changes at the spinal cord level. Moxibustion was applied to the ipsilateral (right) Zusanli (ST36) acupoint to the lesion side for 9 days to CFA-induced arthritic rats. The stepping force was measured as a behavioral test, c-Fos immunohistochemistry, NO production and nNOS Western blots were examined to evaluate antinociceptive effects. Moxibustion at ST36 significantly improved the stepping force in the affected hind limb in CFA-induced arthritis. Moreover, moxibustion at ST36 suppressed the production of NO and the protein expression of c-Fos and nNOS induced by arthritis. These results suggest that moxibustion at ST36 has a potent antinociceptive effect in an arthritic rat model, and modulates neuronal excitability and endogenous NO production by suppressing c-Fos and nNOS protein expression.

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Taranov, O. S., S. N. Yakubitskiy, T. S. Nepomnyashchikh, A. E. Nesterov, and S. N. Shchelkunov. "Adjuvant-Induced Arthritis in Guinea Pigs." Acta Naturae 8, no. 4 (December 15, 2016): 110–17. http://dx.doi.org/10.32607/20758251-2016-8-4-110-117.

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We propose a model of rheumatoid arthritis (RA) induced in outbred guinea pigs using a single subcutaneous injection of complete Freunds adjuvant to the hind paw. Histological examination of this model shows fibrin deposition on the surface of the synovial membrane, leukocyte infiltration of the synovial membrane and adjacent tissues, proliferation of the granulation tissue, and emergence of angioid areas, characteristic of RA. The cell response appears as an increase in the plasma cell count and development of follicle-like lymphoid infiltrates; erosion of the articular surface of the cartilage, frequently with deep cartilage destruction over large areas; and epiphysiopathy. The high reproducibility of arthritis induction in this RA model has been demonstrated. The proposed model is promising for the assessment of anti-arthritis preparations and dosage regimens.

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Patil, Kalpesh Ramdas, Chandragouda Raosaheb Patil, Ramchandra Baburao Jadhav, Vallabh Krishnalal Mahajan, Prabhakar Raosaheb Patil, and Pradeep Sampatrao Gaikwad. "Anti-Arthritic Activity of Bartogenic Acid Isolated from Fruits ofBarringtonia racemosaRoxb. (Lecythidaceae)." Evidence-Based Complementary and Alternative Medicine 2011 (2011): 1–7. http://dx.doi.org/10.1093/ecam/nep148.

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The fruits ofBarringtonia racemosaare prescribed in the ayurvedic literature for the treatment of pain, inflammation and rheumatic conditions. In present investigation, activity guided isolation of bartogenic acid (BA) and its evaluation in the Complete Freund's Adjuvant (CFA)-induced arthritis in rats is reported. Among the various extracts and fractions investigated preliminarily for carrageenan-induced acute inflammation in rats, the ethyl acetate fraction displayed potent anti-inflammatory activity. Large-scale isolation and characterization using chromatography and spectral study confirmed that the constituent responsible for the observed pharmacological effects was BA. Subsequently the BA was evaluated for effectiveness against CFA-induced arthritis in rats. The results indicate that at doses of 2, 5, and 10 mg kg−1 day−1, p.o., BA protects rats against the primary and secondary arthritic lesions, body weight changes and haematological perturbations induced by CFA. The serum markers of inflammation and arthritis, such as C-reactive protein and rheumatoid factor, were also reduced in the BA-treated arthritic rats. The overall severity of arthritis as determined by radiological analysis and pain scores indicated that BA exerts a potent protective effect against adjuvant-induced arthritis in rats. In conclusion, the present study validates the ethnomedicinal use of fruits ofB. racemosain the treatment of pain and inflammatory conditions. It further establishes the potent anti-arthritic effects of BA. However, additional clinical investigations are needed to prove the efficacy of BA in the treatment of various immuno-inflammatory disorders.

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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

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Li, Mingxin, Lidong Zhai, and Wanfu Wei. "High-Methionine Diet Attenuates Severity of Arthritis and Modulates IGF-I Related Gene Expressions in an Adjuvant Arthritis Rats Model." Mediators of Inflammation 2016 (2016): 1–6. http://dx.doi.org/10.1155/2016/9280529.

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Rheumatoid arthritis, a synthesized form of adjuvant arthritis exhibited throughout many animal species, inhibits liver function and circulation of IGF-I and contributes to the degradation of skeletal muscle mass. One of the primary goals of the present study is determining whether a high-Methionine (high-Met) diet is capable of reducing the adverse effects of arthritis, namely, loss of body mass. Following adjuvant injection, forty arthritic rats were randomly assigned to either a control group with a basal diet or a high-Met group with the same basal diet + 0.5% Methionine. After 14 days all rats were terminated. The high-Met group exhibited an increase in body weight and food intake in comparison with the control group (P<0.05). High-Met diet debilitated arthritis-induced surges in the gastrocnemius in both atrogin-1 and the MuRF1 expressions; however, it was observed to have little to no effect on atrogin-1 and MuRF1 gene expression in soleus. At the same time, high-Met diet rats experienced a rise in IGF-I, with lowering of IGFBP-3 gene expression in the gastrocnemius and the soleus. These data suggest that arthritis severity can be partly attenuated by high-Met diet.

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Liu, Yan-li, Hai-ming Lin, Rong Zou, Jun-chao Wu, Rong Han, Laurence N. Raymond, Paul F. Reid, and Zheng-hong Qin. "Suppression of complete Freund's adjuvant-induced adjuvant arthritis by cobratoxin." Acta Pharmacologica Sinica 30, no. 2 (January 26, 2009): 219–27. http://dx.doi.org/10.1038/aps.2008.20.

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Southwood, T. R., R. E. Petty, and J. B. Bradley. "Adjuvant arthritis and peritoneal macrophage activation." Pathology 22 (1990): 33. http://dx.doi.org/10.1016/s0031-3025(16)36417-0.

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Southwood, T. R., R. E. Petty, and J. B. Bradley. "Adjuvant arthritis and peritoneal macrophage activation." Pathology 22 (1990): 35. http://dx.doi.org/10.1016/s0031-3025(16)36426-1.

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KNIGHT, B., D. R. KATZ, D. A. ISENBERG, M. A. IBRAHIM, S. PAGE, P. HUTCHINGS, R. S. SCHWA RTZ, and A. COOKE. "Induction of adjuvant arthritis in mice." Clinical & Experimental Immunology 90, no. 3 (June 28, 2008): 459–65. http://dx.doi.org/10.1111/j.1365-2249.1992.tb05868.x.

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Silván, Ana María, Maria José Abad, Paulina Bermejo, Angel María Villar, and Juan Pedro López-Bote. "Aggravation of adjuvant arthritis by carrageenan." General Pharmacology: The Vascular System 27, no. 4 (June 1996): 639–42. http://dx.doi.org/10.1016/0306-3623(95)02091-8.

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Harbuz, M. S., R. G. Rees, and S. L. Lightman. "HPA axis responses to acute stress and adrenalectomy during adjuvant-induced arthritis in the rat." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 264, no. 1 (January 1, 1993): R179—R185. http://dx.doi.org/10.1152/ajpregu.1993.264.1.r179.

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Adjuvant-induced arthritis results in chronic activation of the hypothalamo-pituitary-adrenal (HPA) axis. In the Piebald-Viral-Glaxo (PVG) rat, however, corticotropin-releasing factor (CRF) mRNA in the parvocellular paraventricular nucleus (pPVN) of the hypothalamus was reduced, and the normal corticosterone and CRF mRNA responses to acute stress were inhibited. The proenkephalin A mRNA response to stress in the pPVN was maintained, implying a specific inhibition of the CRF mRNA responses in this pathological situation. Adrenalectomy at day 0 (the time of adjuvant injection), day 13 (just before inflammation), or day 19 (submaximal inflammation) resulted in a marked increase in CRF mRNA compared with day 21 adrenal-intact arthritic animals. However, levels were below those of nonarthritic adrenalectomized rats, demonstrating that the inhibition of CRF mRNA associated with arthritis is not simply due to changes in glucocorticoid feedback. Proopiomelanocortin mRNA in the anterior pituitary was markedly increased in all adrenalectomized arthritic animals above the increase seen in sham-adrenalectomized day-21 arthritic rats. Adrenalectomy was always associated with an increase in the severity of the disease.

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Kothavade, Pankaj S., Vipin D. Bulani, Dnyaneshwar M. Nagmoti, Padmini S. Deshpande, Nitin B. Gawali, and Archana R. Juvekar. "Therapeutic Effect of Saponin Rich Fraction ofAchyranthes asperaLinn. on Adjuvant-Induced Arthritis in Sprague-Dawley Rats." Autoimmune Diseases 2015 (2015): 1–8. http://dx.doi.org/10.1155/2015/943645.

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Objective. Achyranthes asperaLinn. (AA) is used in folklore for the treatment of various inflammatory ailments and arthritis like conditions. Anti-inflammatory activity of saponin rich (SR) fraction of AA has been previously reported. The objective of this study was to assess the antiarthritic effect of SR fraction ofAchyranthes asperain adjuvant-induced arthritic rats.Methods.Arthritis was assessed by arthritis score, paw volume, changes in tibiotarsal joint thickness, hyperalgesic parameters, and spleen and thymus index. Haematological, serum, biochemical, and inflammatory cytokine andin vivoantioxidant parameters were measured on the last day of the study.Results.SR fraction significantly suppressed paw swelling and arthritic score and improved the pain threshold in motility and stair climbing tests. There was a reversal in the levels of altered parameters, alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and antioxidant parameters like superoxide dismutase, catalase, glutathione, malondialdehyde, and nitric oxide. SR fraction significantly decreased plasma levels of tumor necrosis factor-alpha and interleukin-6. Moreover, histopathology revealed a significant reduction in synovial hyperplasia, inflammatory cell infiltration, and bone destruction in the joints.Conclusion.These observations explain the therapeutic benefit of SR fraction of AA in suppressing the progression of adjuvant-induced arthritis in rats.

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Taurog, J. D., S. S. Kerwar, R. A. McReynolds, G. P. Sandberg, S. L. Leary, and M. L. Mahowald. "Synergy between adjuvant arthritis and collagen-induced arthritis in rats." Journal of Experimental Medicine 162, no. 3 (September 1, 1985): 962–78. http://dx.doi.org/10.1084/jem.162.3.962.

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Adjuvant arthritis (AA) in rats is susceptible to cell-mediated passive transfer. Collagen-induced arthritis (CIA) in rats is susceptible to passive transfer with antibody to type II collagen. We report here the development of strikingly severe arthritis in Lewis rats as the result of synergy between passively transferred antibody to type II collagen from rats with CIA and concanavalin A (Con A)-stimulated lymph node or spleen cells from syngeneic rats with AA. Similar synergy was seen in rats with AA given anticollagen antibody, in rats with CIA given Con A-stimulated adjuvant spleen cells, and in rats actively immunized with CII and complete Freund's adjuvant. The synergistic process caused a very severe polyarthritis, characterized by marked swelling and erythema in all the joints of the distal extremities, with histologic and radiographic evidence of early, extensive erosion of articular cartilage. Synergy was apparent if the lymphoid cells from AA rats were given up to 1 mo after a single injection of anticollagen antibody. No synergy was seen when normal rat immunoglobulin or anti-ovalbumin antibody was substituted for anticollagen antibody, when Con A-stimulated lymphoid cells from normal rats or donors with CIA were used, or when Con A-stimulated AA lymphoid cells were irradiated before transfer. Synergy between separate immune effector mechanisms may represent a general phenomenon in the pathogenesis of inflammatory joint disease.

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Billingham, M. E., S. Carney, R. Butler, and M. J. Colston. "A mycobacterial 65-kD heat shock protein induces antigen-specific suppression of adjuvant arthritis, but is not itself arthritogenic." Journal of Experimental Medicine 171, no. 1 (January 1, 1990): 339–44. http://dx.doi.org/10.1084/jem.171.1.339.

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A recombinant (r)65-kD protein from Mycobacterium leprae, at levels far in excess of those present in whole mycobacteria, was unable to induce arthritis. Even when combined with a synthetic adjuvant, CP20961, to mimic the peptidoglycan adjuvant component of the mycobacterial cell wall, the r65-kD protein failed to induce arthritis. Pretreatment with as little as 1 microgram r65-kD protein protected rats against arthritis induced by M. tuberculosis, but this r65-kD protein was markedly less able to protect against arthritis induced by the synthetic adjuvant, CP20961, or type II collagen. The r65-kD protein appears, therefore, to produce an antigen-specific protection against arthritis induced by bacterial cell walls containing the 65-kD protein. Such protection can be overcome, however, by arthritogenic T lymphocytes, suggesting that protection occurs by preventing clonal proliferation of autoreactive T lymphocytes that are induced by the adjuvant properties of mycobacterial cell walls. How the r65-kD protein abrogates this particular adjuvant activity, and the nature of the arthritogenic self antigen(s), remain to be elucidated.

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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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Warriar, Purnima, Kalyani Barve, and Bala Prabhakar. "Anti-Arthritic Effect of Garcinol Enriched Fraction Against Adjuvant Induced Arthritis." Recent Patents on Inflammation & Allergy Drug Discovery 13, no. 1 (August 5, 2019): 49–56. http://dx.doi.org/10.2174/1872213x12666181120091528.

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Background: Garcinia indica also known as kokum is used in traditional system of medicine for relieving inflammation and rheumatic pain. Garcinol, a benzophenone obtained from its fruit rind is reported to have anti-inflammatory effect via modulating arachidonic acid metabolism, suppressing iNOS expression, NF-κB activation and COX-2 expression. It has also been studied for antioxidant and anticancer activity. Apart from these, few patents claim that garcinol also has anti-obesity and hepatoprotective effect and has a potential to be used for the treatment of renal disorders, endometriosis and cardiac dysfunction. Objective: Garcinol Enriched Fraction (GEF) from the fruit rind of Garcinia indica should be effective in the treatment of arthritis, one of the chronic inflammatory disorder owing to its anti-inflammatory property as indicated by earlier experiments. Methods: GEF was prepared from the fruit rind of Garcinia indica and quantified using LC-MS/MS. It was found to contain 89.4% w/w of garcinol. GEF was evaluated at the dose of 10mg/kg for its efficacy against Complete Freund’s Adjuvant (CFA) induced arthritis in Wistar albino rats. Paw volumes of both sides were measured by Plethysmometer and body weight was recorded on 0, 1, 5, 12 and 21st day. The hyperalgesic response was also measured by motility test and stair climbing test. Results: GEF showed a significant reduction in paw swelling (p < 0.0001) and arthritis index (p < 0.0001) exhibiting anti-inflammatory potential. It also improves the motility and stair climbing ability of experimental animals (p < 0.05), thus reducing hyperalgesia. Conclusion: Garcinol enriched fraction shows anti-arthritic activity in experimental animals.

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Nandhagopal, K., and M. Kanniyakumari. "EFFECT OF RASA MEZHUGU ON FREUND’S ADJUVANT-INDUCED ARTHRITIS IN RATS." International Journal of Current Pharmaceutical Research 8, no. 4 (October 18, 2016): 80. http://dx.doi.org/10.22159/ijcpr.2016v8i4.15686.

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Objective: Rheumatoid arthritis is a long-lasting autoimmune disorder that primarily affects joints. It typically results in warm, swollen, and painful joints. Pain and stiffness often worsen the following rest. The goal of treatment is to reduce pain, decrease inflammation, and improve a person's overall functioning. In spite of tremendous development in the field of synthetic drugs during recent years, the side effects could not be avoided. Hence the current research focus is to develop less toxic drugs as early as feasible in the disease process.Methods: A 90 d old Wistar male rat was used for the research and was divided into four groups treated with Saline, Palm Jaggary, Rasa Mezhugu and Indomethacin.Results: Acute toxicity study, Sub Acute study, Anti-arthritic study and histological findings showed that the Rasa Mezhugu has an anti-arthritis effect.Conclusion: Further the histopathology slide photos of bone, cerebrum, cardiac muscle, kidney, liver, pancreas, ovaries, lungs, testes, stomach and spleen proved the safety of Rasa Mezhugu in rats.

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Castillero, Estíbaliz, Ana Isabel Martín, María López-Menduiña, Maria Angeles Villanúa, and Asunción López-Calderón. "Eicosapentaenoic acid attenuates arthritis-induced muscle wasting acting on atrogin-1 and on myogenic regulatory factors." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 297, no. 5 (November 2009): R1322—R1331. http://dx.doi.org/10.1152/ajpregu.00388.2009.

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Eicosapentaenoic acid (EPA) is an omega-3 polyunsaturated fatty acid that has anti-inflammatory and anticachectic actions. The aim of this work was to elucidate whether EPA administration is able to prevent an arthritis-induced decrease in body weight and muscle wasting in rats. Arthritis was induced by intradermal injection of Freund's adjuvant; 3 days later, nine rats received 1 g/kg EPA or coconut oil daily. All rats were killed 15 days after adjuvant injection. EPA administration decreased the external signs of arthritis and paw volume as well as liver TNF-α mRNA. EPA did not modify arthritis-induced decrease in food intake or body weight gain. However, EPA treatment prevented arthritis-induced increase in muscle TNF-α and atrogin-1, whereas it attenuated the decrease in gastrocnemius weight and the increase in MuRF1 mRNA. Arthritis not only decreased myogenic regulatory factors but also increased PCNA, MyoD, and myogenin mRNA in the gastrocnemius. Western blot analysis showed that changes in protein content followed the pattern seen with mRNA. In the control rats, EPA administration increased PCNA and MyoD mRNA and protein. In arthritic rats, EPA did not modify the stimulatory effect of arthritis on these myogenic regulatory factors. The results suggest that in experimental arthritis, in addition to its anti-inflammatory effect, EPA treatment attenuates muscle wasting by decreasing atrogin-1 and MuRF1 gene expression and increasing the transcription factors that regulate myogenesis.

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Kwon, Ki Sun, Hyun Lim, Yong Soo Kwon, Hye Ri Choi, Myong Jo Kim, Ji Hye Yoo, Nam Ho Yoo, and Hyun Pyo Kim. "Anti-arthritic Effects of Oplopanax elatus in a Rat Model of Rheumatoid Arthritis (Adjuvant-induced Arthritis)." Natural Product Sciences 25, no. 4 (2019): 304. http://dx.doi.org/10.20307/nps.2019.25.4.304.

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Živná, Helena, Ljiljana Maric, Iveta Gradošová, Klára Švejkovská, Soňa Hubená, and Pavel Živný. "The Effect of Mud-Bath Therapy on Bone Status in Rats During Adjuvant Subchronic Arthritis." Acta Medica (Hradec Kralove, Czech Republic) 55, no. 3 (2012): 133–37. http://dx.doi.org/10.14712/18059694.2015.51.

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Introduction: We studied influence of mud-bath on bone status in male Wistar rats with subchronic arthritis. Methods: Arthritis was induced by 2 subplantar injections of Freund’s adjuvans with heat-killed Streptoccocus pyogenes into paw. Groups: intact (int) on chippings; (con) arthritis on chippings; (san38) arthritis on hot sand; (mu38) arthritis on hot mud; (mu21) arthritis on mild mud. Bone mineral density (BMD, g/cm2) was measured by dual energy X-ray absorptiometry and femurs were tested biomechanically. Bone markers osteocalcin (OC), PINP and CTX were analysed in bone. Results: BMD of right femur decreased vs. left in san38 (p = 0.030) and mu38 (p = 0.047). Fracture load of right/left femur (N) decreased in experimental groups, significantly in san38 (p = 0.05). Fracture threshold of neck decreased in right vs. left in experimental groups, but significantly in san38 (p = 0.05). OC decreased in mu38 vs. con (1.84 ± 0.14/2.62 ± 0.23). PINP decreased in int vs. san38 (p = 0.005) and mu21 (p < 0.001). CTX decreased in int vs. mu38 (p = 0.006) and mu21 (p = 0.005). Conclusion: The hot bath appears indifferent in relation to osteoporosis, while cold mud-bath shows good effect on bone metabolism. The cold mud-baths help to reduce arthritic inflammation and pain and thereby lead to higher mobility with positive consequence on bone.

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Lima, Mariana Machado, Lorena Gimenes da Silva, Jailson Araújo Dantas, Ciomar Aparecida Bersani Amado, Miguel Spack Junior, and Jacqueline Nelisis Zanoni. "Evaluation of the effects of autohemotransfusion in arthritic rats induced by two doses of complete Freund´s adjuvant." Acta Scientiarum. Biological Sciences 41, no. 1 (April 16, 2019): 36978. http://dx.doi.org/10.4025/actascibiolsci.v41i1.36978.

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The aim the study was to evaluate the effects of autohemotransfusion in adjuvant-induced arthritis model by injections of high and low doses of Complete Freund´s Adjuvant (CFA). Male Holtzman rats (200-230g) were distributed in six groups: control (C); control treated by autohemotransfusion (CT); CFA induced arthritis 0.5% w/v (AIA); CFA induced arthritis 0.5% w/v treated with autohemotransfusion (AIAT); CFA induced arthritis 0.1% w/v (AS) and CFA induced arthritis 0.1% w/v treated with autohemotransfusion (AST). The number of leukocytes, the weight of different organs and the paw volume were analyzed. The autohemotransfusion without erythrocytes promoted a reduction in the number of leukocytes in AIAT and AST when compared to AIA (p < 0.001). In the AST group an increase of the thymus weight (p < 0.05) was observed when compared to C, AIA and AIAT. The autohemotransfusion did not prevent the occurrence of paw edema in arthritic animals of AIAT and AST groups (p>0.05). The autohemotransfusion used in this work presented positive effects on AIA as they promoted a reduction in the number of leukocytes and an increase in thymus weight and body growth. However, other types of autohemotransfusion must be tested to determine the true efficacy of this alternative method of treatment.

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Karthik, R., D. Arul Ananth, N. Gayathri, L. Dinesh Kumar, and T. Sivasudha. "Evaluation of Anti-arthritic Potential of Pisonia grandis R. Br Against Complete Freund’s Adjuvant (CFA) Induced Albino Wistar Rats." Phytothérapie 16, S1 (December 2018): S96—S103. http://dx.doi.org/10.3166/phyto-2018-0078.

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Medicinal plants have been employed in the treatment of human ailments since time immemorial. Arthritis is a joint disorder affecting the subchondral bone and cartilage. The continuous action of reactive oxygen species and inflammatory mediators are also reported to cause further damage to the joints by immunological activation. DriedPisonia grandisleaves were powdered for the extraction process. Albino Wistar rats were randomly divided into five groups with six animals in each group. Groups IV and V were complete Freund’s adjuvant (CFA) induced arthritic rats which receivedPisonia grandisethanol extract (PGEE; 250 and 500 mg/kg b.w. [body weight]) respectively from 15th to 35th day of induction of CFA induced arthritis. PGEE protects rats against primary and secondary arthritic lesions, body weight changes, and hematological perturbations induced by CFA. The serum markers of inflammation and arthritis, such as C-reactive protein and rheumatoid factor, were also reduced in the PGEE-treated arthritic rats. High performance liquid chromatography (HPLC) and tandem mass spectrometry (MS/MS) analysis of PGEE detected the presence of polyphenolic compounds such as resveratrol, quercetin, and naringenin. The study confirmed that presence of bioactive phytocompounds in ethanolic extract ofPisonia grandisR. Br. Overall, PGEE was observed to be a potent agent reducing arthritis-mediated cartilage/bone degradation, inflammation, and associated stress in vivo, which gives cause for further research.

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Chaudhary, Sushma, Manjul Pratap Singh, Chandana Venkateaswara Rao, and Ajay Kumar Singh Rawat. "A Novel Natural Polymers Based Nanoparticles Gel Formulation for the Treatment of Rheumatoid Arthritis: Optimization and In-vivo Evaluation." Drug Delivery Letters 11, no. 2 (June 28, 2021): 164–78. http://dx.doi.org/10.2174/2210303111666210219152401.

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Background: In 1988, the US Food and Drug Administration permitted low dose methotrexate for the treatment of rheumatoid arthritis that would change the progression of the disease. Methotrexate is a folic acid antagonist and its systemic use causes numerous side effects; including hepatic toxicity. It would be preferable to deliver methotrexate by the topical route to reduce side-effects along with ease of administration and reduced dosing frequency. So, nanoparticle gel is a hopeful approach to treat rheumatoid arthritis. Objective: The study aims to develop a nanoparticles gel containing novel natural polymer-based methotrexate nanoparticles and evaluate its therapeutic potential on Complete Freund’s Adjuvant– Induced Arthritis rat model and compare it to methotrexate and dexamethasone gel. Materials and Methods: The five batches of methotrexate nanoparticles gel were prepared viz. F1W2, F2W2, F3W2, F4W2 and methotrexate gel for the topical application by using different concentrations of Carbopol 934 base and characterized for their evaluation parameters: homogeneity, grittiness, pH, spread-ability, viscosity determination, and drug content studies. The arthritic potential of methotrexate-nanoparticles gel was evaluated by Complete Freund’s Adjuvant–Induced Arthritis rats model based on percent inhibition oedema and arthritic score. Result and Discussion: Methotrexate nanoparticles gel significantly reduced the percentage inhibition of oedema compared to methotrexate and dexamethasone gel. The therapeutic activity of nanoparticles gel was found to be F3W2 ≥ F2W2 ≥ F1W2 ≥ F4W2 ≥ MTX gel. So, the optimized nanoparticle gel formulation F3W2 can be effective in the treatment of rheumatoid arthritis. Conclusion: The developed novel nanoparticles gel formulation can be a promising alternative to existing methotrexate and dexamethasone gel.

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Journal articles on the topic 'Adjuvant arthritis'

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