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目的评价通痹合剂乙酸乙酯部位(TBHJ)对胶原诱导型关节炎(CIA)大鼠的影响,揭示其抗炎抗风湿的作用机制。方法牛Ⅱ型胶原混合弗氏完全佐剂于Wistar大鼠尾根部注射造模,随机分为模型组,甲氨蝶呤(MTX)组和TBHJ治疗组,容积法评价后肢肿胀度;给药后30 d,乳腺钼靶机大鼠四肢摄片,计分法评价各组大鼠X光片四肢96块骨侵蚀和100个关节间隙变化;处死动物,取后肢踝关节苏木素-伊红染色,观察中性粒细胞、淋巴细胞和浆细胞浸润,滑膜细胞增生和软骨破坏的情况;免疫组化法观察关节内IL-17和CD28表达;RT-PCR法比较CD28 mRNA表达。结果 CIA大鼠出现严重的关节炎症和破坏,TBHJ给药后7 d即可明显抑制CIA大鼠关节肿胀;给药后30 d,TBHJ和MTX可明显抑制大鼠关节肿胀和关节破坏,与模型组比较有统计学差异(P<0.01);TBHJ可明显抑制CIA大鼠中性粒细胞、淋巴细胞、浆细胞的浸润、滑膜增生和软骨破坏(P<0.05),MTX可抑制滑膜增生和软骨破坏;CIA大鼠IL-17,CD28 mRNA和蛋白表达明显增加,TBHJ可明显抑制IL-17和CD28。结论 TBHJ具有抑制关节免疫炎症和关节破坏的作用,其机制可能是通过抑制T细胞第二信号分子CD28的表达,减少IL-17的产生实现的。
Objective To evaluate the effect of Tongbi Mixture’s ethyl acetate fraction (TBHJ) on collagen-induced arthritis (CIA) in rats and its anti-inflammatory and antirheumatic mechanism. Methods Cattle Ⅱ Collagen mixed Freund’s complete adjuvant was injected into the caudal root of Wistar rats and randomly divided into model group, methotrexate (MTX) group and TBHJ treatment group. The volumetric method was used to evaluate the swelling degree of hind limbs. After administration 30 days. Mammograms of the mammograms were used to evaluate the bone erosions and the changes of the articular spaces in 96 limbs of X-ray films of all groups. The animals were sacrificed and the hematoxylin-eosin The infiltration of neutrophils, lymphocytes and plasma cells, synovial cell proliferation and cartilage destruction were observed. The expression of IL-17 and CD28 in the joints was observed by immunohistochemistry. The expression of CD28 mRNA was detected by RT-PCR. Results Severe joint inflammation and destruction were found in CIA rats. Joint swelling was found in CIA rats 7 d after TBHJ administration. At 30 d after TBHJ treatment, TBHJ and MTX significantly inhibited joint swelling and joint destruction, (P <0.01). TBHJ could significantly inhibit the infiltration of neutrophils, lymphocytes and plasma cells, synovial hyperplasia and cartilage destruction in CIA rats (P <0.05). MTX could inhibit synovial hyperplasia And cartilage destruction. The mRNA and protein expressions of IL-17 and CD28 in CIA rats were significantly increased. TBHJ could significantly inhibit IL-17 and CD28. Conclusion TBHJ can inhibit joint immune inflammation and joint destruction, and its mechanism may be through inhibiting the expression of CD28, the second signal molecule of T cells and reducing the production of IL-17.