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目的探讨中药通痹灵在类风湿关节炎(RA)发病中对软骨细胞凋亡及其基因p53、Bcl2调控的作用机制。方法采用大鼠CIA模型,分别予通痹灵、甲氨蝶呤片(MTX)、雷公藤治疗36d,关节软骨免疫组化染色,计算机图像分析系统对软骨p53、Bcl2基因蛋白及细胞凋亡的表达进行分析,比较各组差异。结果CIA大鼠软骨细胞中存在高度活跃的p53蛋白表达,通痹灵可以下调细胞中过度活跃的p53蛋白表达,MTX高剂量及雷公藤高剂量的作用不显著;大鼠软骨细胞Bcl2蛋白表达呈抑制状态,通痹灵低剂量组明显上调Bcl2蛋白的低表达水平,其次为雷公藤高剂量组;大鼠软骨细胞存在明显的凋亡亢进,通痹灵明显下调细胞凋亡水平。结论通痹灵能通过调整过度表达的p53蛋白与低表达的Bcl2蛋白,抑制软骨细胞的过度凋亡;MTX与雷公藤对凋亡的作用与Bcl2基因家族的调控密切相关,与p53相关基因的相关性不显著。
Objective To investigate the mechanism of Tongfuling, a traditional Chinese medicine, on the apoptosis of chondrocytes and the regulation of p53 and Bcl2 genes in the pathogenesis of rheumatoid arthritis (RA). Methods The rat CIA model was used to treat 36 days of Tongfuling, MTX and Tripterygium wilfordii, and the articular cartilage was immunohistochemically stained. The computer image analysis system was used to detect the p53, Bcl2 gene protein and apoptosis of cartilage. Express the analysis and compare the differences. Results There was highly active p53 protein expression in chondrocytes of CIA rats. Tongbiling could down-regulate the expression of overactive p53 protein in the cells. The effect of high dose of MTX and high dose of Tripterygium wilfordii was not significant; the expression of Bcl2 protein was inhibited in rat chondrocytes. In the low-dose Tongweiling group, the expression of Bcl2 protein was significantly up-regulated, followed by the high-dose group of Tripterygium wilfordii; the chondrocytes in rats exhibited significant apoptosis, and Tongfuling significantly down-regulated the apoptosis. Conclusion Tongbi Ling can inhibit excessive apoptosis of chondrocytes by over-expressing p53 protein and low expression of Bcl2 protein; the effect of MTX and Tripterygium wilfordii on apoptosis is closely related to the regulation of Bcl2 gene family, and related to p53 gene. The correlation is not significant.