Rheumatoid arthritis (RA) is a chronic and accelerated autoimmune illness with proliferative and damaging synovitis, resulting in joint death and cartilage and bone erosion. This study focused on the potential therapeutic effect of wogonin on complete Freund's adjuvant (CFA) induced RA in rats and the underlying mechanisms. Arthritis was experimentally caused in rats by subcutaneously injecting 0.1 mL of CFA into the subplantar area of the left hind paw under moderate anesthesia on day zero. The regular oral doses of indomethacin/wogonin began on day zero and proceeded after injection to day 35. Wogonin reduced arthritic score considerably, enhanced body weight, and reduced paw thickness. Wogonin also boosted red blood cell considerably along with hemoglobin and reduced white blood cell count and erythrocyte sedimentation rate. Wogonin substantially improved an altered level of oxidative stress markers, antioxidant proteins, and inflammatory cytokines in a dose‐dependent way. Wogonin inhibited p38 phosphorylation triggered by CFA and p65 nuclear translocation.

中文翻译：

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Wogonin通过靶向NF-κB/ MAPK信号通路改善了完全的弗氏佐剂诱导的类风湿关节炎。

类风湿关节炎（RA）是一种慢性，加速的自身免疫性疾病，具有增生性和破坏性滑膜炎，可导致关节死亡，软骨和骨侵蚀。这项研究的重点是沃戈宁对完全弗氏佐剂（CFA）诱导的大鼠RA的潜在治疗作用及其潜在机制。在实验的第0天，在中度麻醉下，将0.1 mL CFA皮下注射到左后爪的足底下区域，从而在实验中引起了关节炎。消炎痛/ Wogonin的常规口服剂量在第0天开始，并在注射后一直持续到第35天。Wogonin显着降低了关节炎评分，增加了体重，并减少了脚掌的厚度。沃戈宁还与血红蛋白一起极大地促进了红血球的产生，并减少了白血球数量和红细胞沉降率。Wogonin以剂量依赖的方式显着改善了氧化应激标志物，抗氧化剂蛋白和炎性细胞因子水平的改变。Wogonin抑制了CFA和p65核易位触发的p38磷酸化。