Mechanism of Resveratrol Improving Rheumatoid Arthritis Injury by Inhibiting S100A8/A9 Expression

Abstract

To investigate whether calprotectin is involved in the protective effect of resveratrol on rheumatoid arthritis injury and its potential mechanism. 12 of the 72 rats were randomly selected as blank group; rheumatoid arthritis model was constructed by bovine collagen II complete Freund's adjuvant method. The rats with successful modeling were divided into model group, high, medium and low-dose resveratrol groups (60, 30, and 15 mg/kg), and toll-like receptor 4 agonist (neoseptin 3) group (resveratrol 60 mg/kg+neoseptin 3 1 mg/kg), with 12 rats in each group. Each group was intervened by gavage of corresponding drugs once a day for 42 d. The general state of the rats was observed; the rat ankle joint volume was detected and the swelling degree was calculated; rats were scored for arthritis index; serum levels of interleukin 6, tumor necrosis factor-alpha and interleukin 1 beta contents were measured by enzyme-linked immunosorbent assay; the histological changes of ankle joints were observed by hematoxylin and eosin staining; calprotectin, toll-like receptor 4 and nuclear factors-kappa B p65 protein expression in ankle tissues were determined by Western blot analysis. The rats in resveratrol group had good mental state, significantly reduced joint swelling, increased body weight, decreased inflammatory cell infiltration and new pannus in synovial tissue, the joint swelling rate, arthritis index, serum tumor necrosis factor-alpha, interleukin 6 and interleukin 1 beta contents, calprotectin, toll-like receptor 4, nuclear factors-kappa B p65 protein expression in ankle joint tissue were significantly lower (p<0.05); in a dose-dependent manner. Neoseptin 3 can reverse the protective effect of resveratrol on rheumatoid arthritis rats. Resveratrol may inhibit calprotectin expression, which in turn may inhibit the activation of toll-like receptor 4/nuclear factors-kappa B p65 signaling pathway, thereby exerting a protective effect on rheumatoid arthritis rats.