【摘要】 目的 :观察中药金三莪抗大鼠肝纤维化的疗效及作用机制。方法 :采用金三莪治疗四氯化碳诱导大鼠肝纤维化模型。RT -PCR检测肝组织TGFβ1、TGFRⅠ与TGFRⅡmRNA ;免疫组化技术检测Smad3及Smad7在肝内的表达及定位 ,肝组织HE染色检测病理改变。结果 :与模型组大鼠比较 ,RT -PCR显示经该中药组方治疗 ,大鼠肝内TGFβ1、TGFRⅠ与TGFRⅡmRNA(P <0 .0 5 ,P<0 .0 1) ,以及Smad3表达明显降低 ;而Smad7的表达增加。Smad3的免疫阳性反应信号主要位于纤维间隔中的细胞浆 ,Smad7则主要在肝细胞浆表达。肝小叶结构趋于正常 ,纤维间隔明显变薄。结论 :金三莪组方能有效地减轻肝纤维化大鼠的肝脏损伤及纤维化程度 ,其机理与抑制肝内TGFβ1 、TGFRⅠ与TGFRⅡmRNA及Smad3表达 ,并促进Smad7表达有关。更多还原

【Abstract】 Object:To investigate the effect and mechanism of the JinSanE on hepatic fibrosis induced in rats. Methods:50 Wistar rats were randomly allocated into four study groups:group A was healthy controls,group B was CCl 4 induced rats, group C and D were CCl 4 induced rats treated with JinSanE starting at the first and fourth week since rat exposured CCl4. Rats were killed and blood and liver were collected for further determinations at the eighth week. The effect of JinSanE was evaluated of the level of transforming growth factor-beta1(TGFβ 1), TGFRⅠand TGFRⅡmRNA by RT-PCR, the expressions and sites of TGF-β 1, Smad3 and Smad7 in liver tissue by immuneohistochemistry attaining, the liver histopathology was also examined by HE stainings. Results:Compared with the group B, the level of TGFβ 1,TGFRⅠ, TGFRⅡ mRNA and the expression Smad3 were significantly decreased in group C and group D, and the expression of Smad7 was also remarkable increased in liver of rats treated with JinSanE (P<0.05 or P<0.01). The histological changes of fibrosis were also obviously improved. Conclusion:The JinSanE has protective effect on liver injury and can inhibit hepatic fibrosis induced by CCl4 in rats. The mechanisms possibly associated with their effect of down-regulating TGF-β 1 TGFRⅠ, TGFRⅡ mRNA and smad3, up-regulating Smad7 and resulted in suppressing the activation of hepatic stellate cells.更多还原