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目的:观察川芎嗪对大鼠实验性肝纤维化作用的治疗效果,并探讨其作用机制。方法:采用四氯化碳(CCL4)诱导大鼠肝纤维化模型,将实验动物随机分为正常对照组(N)5只、肝纤维化模型组(H)20只、川芎嗪治疗组(TM P)20只,除正常对照组以外其它两组均给予40%四氯化碳(CCL4)花生油溶液0.3m l/100g腹腔注射,每周2次,共6周。川芎嗪组于肝纤维化模型建立后给予盐酸川芎嗪(TM P)60m g/kg经口灌胃,1次/d,连续治疗60天;其余两组同时给予同等剂量的生理盐水。于60天后分别处死各组大鼠。用HE石蜡组织切片观察各组光镜下肝组织结构变化;用免疫组织化学方法染色观察肝组织中I型胶原(C o llagen type I,C oI)表达的变化,并利用计算机图像分析技术测量正常对照组、肝纤维化模型组及川芎嗪治疗组C oI表达的平均光密度。结果:免疫组织化学S-P法染色显示TM P能明显抑制肝组织中C oI水平的表达,C oI在川芎嗪治疗组中的表达明显低于肝纤维化模型组,C oI在川芎嗪治疗组与肝纤维化模型组之间有显著性差异(P<0.01);C oI在川芎嗪治疗组与正常对照组中呈高表达,C oI在川芎嗪治疗组与正常对照组之间差异无显著性(P>0.05)。结论:川芎嗪对四氯化碳(CCL4)诱导的大鼠实验性肝纤维化有明显的保护和治疗作用。
Objective: To observe the therapeutic effect of tetramethylpyrazine on experimental hepatic fibrosis in rats and to explore its mechanism of action. METHODS: Rat hepatic fibrosis model was induced by carbon tetrachloride (CCL4). The experimental animals were randomly divided into five groups: normal control group (N), liver fibrosis model group (H), and ligustrazine treatment group (TM P) Twenty rats except the normal control group were given 40% carbon tetrachloride (CCL4) peanut oil 0.3 ml/100 g intraperitoneally twice a week for 6 weeks. The Ligustrazine group was given 60 mg/kg of tetramethylpyrazine hydrochloride (TM P) 60 mg/kg once a day after liver fibrosis model was established, and was continuously treated for 60 days. The other two groups were given the same dose of physiological saline at the same time. Rats in each group were sacrificed after 60 days. HE staining was used to observe the changes of liver tissue structure under light microscope; Immunohistochemical staining was used to observe the expression of type I collagen (C oI) in liver tissue and measured by computer image analysis technique. The average optical density of C oI expression in normal control group, hepatic fibrosis model group, and Ligustrazine treatment group. Results: SP immunohistochemistry staining showed that TM P could significantly inhibit the expression of C oI in liver tissue. The expression of C oI in the tetramethylpyrazine treatment group was significantly lower than that in the liver fibrosis model group. The C oI was in the tetramethylpyrazine treatment group. There was a significant difference between the liver fibrosis model group (P<0.01); C oI was highly expressed in the tetramethylpyrazine treatment group and the normal control group, and there was no significant difference in the C oI between the tetramethylpyrazine treatment group and the normal control group. (P>0.05). Conclusion: Tetramethylpyrazine has obvious protective and therapeutic effects on experimental hepatic fibrosis induced by carbon tetrachloride (CCL4) in rats.