甘草酸二铵对肝纤维化实验大鼠TGF-β/Smad信号转导通路相关因子的影响

Effect of diammonium glycyrrhizinate on related factors of TGF-β/Smad signaling pathway in hepatic fibrosis rats

目的初步探讨TGF-β/Smad信号转导通路相关因子TGF-β1、Smad3和Smad7与肝纤维化之间的相关性,以及甘草酸二铵对肝纤维化的干预作用。方法采用皮下注射四氯化碳法构建肝纤维化大鼠模型,实验分为正常对照组,模型对照组,甘草酸二铵组和复方鳖甲软肝片组;运用实时荧光定量RTPCR法检测各组大鼠肝组织TGF-β1、Smad3和Smad7 mRNA的表达变化,Western Blot法检测各组大鼠肝组织TGF-β1、Smad3和Smad7蛋白的表达变化。结果模型对照组与正常对照相比,TGF-β1和Smad3mRNA和蛋白的表达明显升高,Smad7蛋白的表达降低,差异具有统计学意义(P<0.05或P<0.01);给药各组与模型组相比,TGF-β1和Smad3 mRNA和蛋白的表达明显降低,Smad7蛋白的表达增多,差异具有统计学意义(P<0.05或P<0.01)。结论 TGF-β/Smad信号转导通路的激活促进肝纤维化的形成发展,给予甘草酸二铵干预后,可有效抑制TGF-β/Smad信号转导通路的活化,进而对肝纤维化起到保护作用,为防治肝纤维化提供新的作用靶点。

Objective Preliminary study on the correlation between related factors of TGF-β/Smad signal pathway and liver fibrosis. Methods Liver fibrosis model rat was induced by intraperitoneal injection of 40% CC14（0.5ml/100g）, Sprague-Dawley rats were randomly divided into normal control group, model group, diammonium glycyrrhizinate group, and Fufangbiejiaruangan Tablet group. RT-PCR and Western Blot for TGF- β1, Smad3 and Smad7. Results Compared with and protein expression all increased, Smad7 gene normal control group, model group TGF-β1 and Smad3 gene and protein expression decreased, with significant difference （P 〈0. 05 or P 〈 0.01 ） ; Compared with model group, the drug groups TGF-β1 and Smad3 gene and protein expression all decreased, and Smad7 gene and protein expression increased, with significant difference （ P 〈0. 05 or P 〈 0. 01 ）. Conclusions TGF-131/Smad signaling transduction pathway activation promotes the formation and development of liver fibrosis, then diammonium glycyrrhizinate can inhibit TGF-β1/Smad signaling transduction pathway activation effectively, thereby playing a protective role on liver fibrosis, and providing a new target for the prevention and treatment of liver fibrosis.