The purpose of the experiment was to explore the effect of Ganoderic acid A (GAA) on adjuvant-induced arthritis in rats. In this study, the rat model of collagen-induced rheumatoid arthritis (CIA) was established with type II collagen plus Freund's complete adjuvant. Arthritis index, joint pathology, toe swelling, hemorheology, synovial cell apoptosis, related cytokines and JAK3/STAT3 and nuclear factor-κB (NF-κB) signaling pathway were measured in rats. We found that GAA can significantly inhibit the arthritis index, improve joint pathology, reduce toe swelling, improve blood rheology, improve synovial cell apoptosis, and restore related cytokine negative regulation JAK3/STAT3 and NF-κB signaling pathways. In conclusion, GAA has an obvious therapeutic effect on joint inflammation of toes in CIA model rats, which may be due to the regulation of JAK3/STAT3 and NF-κB signaling pathway.

实验的目的是探讨灵芝酸A（GAA）对佐剂诱发的大鼠关节炎的影响。在这项研究中，使用II型胶原蛋白和弗氏完全佐剂建立了胶原蛋白诱发的类风湿关节炎（CIA）大鼠模型。在大鼠中测量关节炎指数，关节病理学，脚趾肿胀，血液流变学，滑膜细胞凋亡，相关细胞因子和JAK3 / STAT3和核因子-κB（NF-κB）信号通路。我们发现，GAA可以显着抑制关节炎指数，改善关节病理，减少脚趾肿胀，改善血液流变学，改善滑膜细胞凋亡，并恢复相关的细胞因子负调控JAK3 / STAT3和NF-κB信号通路。总之，GAA对CIA模型大鼠的脚趾关节发炎具有明显的治疗作用，