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目的:从滑膜新生血管生成的角度,部分揭示祛痹方治疗类风湿关节炎(RA)的作用机制。方法:选用雄性SD大鼠,随机选取12只作为空白对照组,其余60只采用尾根部皮下注射Ⅱ型胶原与不完全弗氏佐剂的方法制作胶原诱导性关节炎(CIA)模型。15d后将CIA大鼠随机分为模型组、雷公藤多苷组、祛痹方高、低剂量组,随即灌胃给药,1次/d,连续4周。采用免疫组化的方法检测大鼠膝关节滑膜组织中fins样酪氨酸激酶(FLT-4)和胎肝激酶受体(FLK-1)的变化。结果:与空白对照组比较,模型组大鼠FLK-1、FLT-4明显升高(P<0.01);雷公藤多苷组和祛痹方高剂量组FLK-1、FLT-4水平较模型组明显降低(P<0.01),且祛痹方高剂量组FLK-1较雷公藤多苷组明显降低(P<0.05)。结论:祛痹方治疗RA的功效与抑制新生血管生成相关。
Objective: From the perspective of synovial neovascularization, the mechanism of Qubei Recipe in the treatment of rheumatoid arthritis (RA) is partially revealed. Methods: Twelve male Sprague-Dawley rats were randomly selected as the blank control group, and the other 60 rats were induced collagen induced arthritis (CIA) by subcutaneous injection of type Ⅱ collagen and incomplete Freund’s adjuvant. After 15 days, CIA rats were randomly divided into model group, tripterygium glycosides group, Qubi Fang high and low dose group, followed by intragastric administration once a day for 4 weeks. Immunohistochemical method was used to detect the changes of fins-like tyrosine kinase (FLT-4) and fetal liver kinase receptor (FLK-1) in synovial tissue of rats. Results: Compared with the blank control group, the levels of FLK-1 and FLT-4 in the untreated group were significantly increased (P <0.01) (P <0.01), and FLK-1 in high-dose Qubi Fang group was significantly lower than that in tripterygium glycosides group (P <0.05). Conclusion: The efficacy of Qubi Recipe in treating RA is related to the inhibition of angiogenesis.