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Rheumatoid arthritis (RA) and its animal model adjuvant arthritis (AA) are inflammatory diseases characterized by chronic inflammation, systemic oxidative stress and disturbed mitochondrial bioenergetics of skeletal muscle. The present study aimed to evaluate the effects of coenzyme Q10 - CoQ10 (100 mg/kg b.w.), omega-3-polyunsaturated fatty acids - 1-3-PUFA (400 mg/kg b.w.) and their combined treatment in AA on impaired skeletal muscle mitochondrial bioenergetics, inflammation and changes in levels CoQ9 and CoQ10 in plasma. Markers of inflammation (C-reactive protein, monocytechemotactic protein-1), antioxidant capacity of plasma, respiratory chain parameters of skeletal muscle mitochondria and concentrations of CoQ9 and CoQ10 in plasma and in muscle tissue were estimated. Treatment of the arthritic rats with CoQ10, 1-3-PUFA alone and in combination partially reduced markers of inflammation and increased antioxidant capacity of plasma, significantly increased concentrations of coenzyme Q in mitochondria and improved mitochondrial function in the skeletal muscle. Combined treatment has similar effect on the mitochondrial function as monotherapies; however, it has affected inflammation and antioxidant status more intensively than monotherapies. Long-term supplementary administration of coenzyme Q10 and 1-3-PUFA and especially their combination is able to restore the impaired mitochondrial bioenergetics and antioxidant status in AA. [ABSTRACT FROM AUTHOR]

Recent studies have demonstrated anti-inflammatory and chondroprotective properties of hyaluronic acid (HA) in rheumatoid arthritis. This study aimed to examine the combination of HA and methotrexate (MTX) in rats suffering from adjuvant arthritis (AA). In our studies, we used male Lewis rats and the arthritis was induced with Mycobacterium butyricum. The experiments included healthy controls, arthritic animals not treated, arthritic animals treated with HA or MTX, and arthritic animals treated with the combination of HA and MTX. Animals received daily doses of 0.5 mg and 5 mg/kg b.w. of HA of varying molecular weights (0.43, 0.99, and 1.73 MDa) alone or combined with MTX in an oral dose of 0.3 mg/kg b.w. twice weekly. We measured improving effect of HA on antioxidant enzymes in erythrocytes (superoxide dismutase and glutathione peroxidase) and on plasma antioxidant capacity. Moreover, we found that HA reduced a marker of oxidative damage of lipids in plasma--the level of lipid hydroperoxides. Most significant was the effect of HA with higher molecular weight. Finally, combined administration of HA and MTX suppressed arthritic progression in rats more effectively than MTX alone. There is a possibility that this finding will lead to improved treatments for rheumatoid arthritis patients. [ABSTRACT FROM AUTHOR]

During rheumatoid arthritis (RA), there is a shift in redox balance. Natural compounds play a major role as an adjuvant in reducing the symptoms of RA. In this study we evaluated the effect of carotenoids (astaxanthin, beta-carotene, and beta-cryptoxanthin) in monotherapy or in combination therapy with methotrexate (MTX) on clinical parameters during adjuvant arthritis (AA). Male Lewis rats were divided into 8 groups. The AA was induced by an injection of Mycobacterium butyricum into the base of the tail. The clinical data were assessed every 7 days until the 28th day. MTX was administrated twice a week (0.3 mg/kg of body weight). Synthetic astaxanthin (ASYN, 20 mg/kg) and natural astaxanthin (ASTAP, 20 mg/kg, source: Blakeslea trispora) were both administrated alone and in combination with MTX. Dosage of beta-carotene was 20 mg/kg and of beta-cryptoxanthin was 10 µg/kg. Administration per os was used. In amelioration of the weight loss caused by arthritis we observed that combination of both astaxanthins with MTX was more effective as MTX alone. Further all carotenoids improved this parameter also in monotherapy. ASTAP had the highest effect. In the most important clinical outcome--changes of the hind paw volume--were all carotenoids effective excluding beta-carotene and ASYN. In conclusion, carotenoids could be a prospective addition to RA therapy. Further evaluation of inflammation and oxidative stress should be aimed. [ABSTRACT FROM AUTHOR]