INF-γ对肝纤维化大鼠TGF-β1/Smad3蛋白表达的影响  

Effect of INF-γ on hepatic fibrosis in rats of TGF-β1/Smad3 protein expression

作　　者：黄越龙[1] 周春光[1] 张谊[1] 张启瑜[1] 汪海清[1] 裴小龙[1] 

机构地区：[1]温州医学院第一附属医院肝胆外科,浙江温州325000

出　　处：《肝胆胰外科杂志》2012年第1期57-59,共3页Journal of Hepatopancreatobiliary Surgery

基　　金：浙江省科技厅资助项目(2010R413034)

摘　　要：目的通过干扰素-γ(IFN-γ)治疗大鼠肝纤维化,观察大鼠肝脏组织病理学及TGF-β1,Smad3蛋白表达水平的变化,探讨INF-γ抗肝纤维化作用机制。方法将48只雄性SD大鼠随机分成对照组、模型组和实验组3组。用3%硫代乙酰胺(TAA)100mg/kg复制大鼠肝纤维化模型,实验组同时肌肉注射INF-γ5U/d。在肝纤维化诱导第8周处死,用Masson染色观测肝组织纤维化程度,免疫组化法检测肝组织TGF-β1、Smad3蛋白表达水平。结果实验组肝纤维化程度、TGF-β1和Smad3表达比正常组增高(P<0.05),比模型组显著降低(P<0.05)。结论 IFN-γ可能通过抑制TGF-β1/Smad3蛋白的表达,从而起到抗肝纤维化的作用。Objective To observe the INF-γ on hepatic fibrosis and changes of TGF-β 1,Smad3 protein expression,and explore the mechanism of INF-γ in treating hepatic fibrosis.Methods Male SD rats were divided into three groups,model group and experimental group were injected with thioacetamide（thioacetamide,TAA） 100 mg/kg,2 days by intraperitoneal injection to induce rat hepatic fibrosis,The control grounp was injected with equal amount of physiological saline,while the experimental group treated with INF-γ intramuscularly.Model group and control group injected with equal physiological saline.All rats were sacrificed at 8 weeks,stained with Masson to observate hepatic fibrosis,detected TGF-β 1,Smad3 protein levels with immunohistochemistry in hepatic tissue.Results The degree of experimental group hepatic fibrosis,the expression of TGF-β1,Smad3 was higher than that in the normal group（P 0.05）,significantly lower than that in the model group（P 0.05）.Conclusion IFN-γ may inhibit TGF-β1/Smad3 protein expression,and thus play a role in hepatic fibrosis.

关 键 词：肝纤维化 干扰素Γ 转化生长因子Β1 SMAD3 信号转导 

分 类 号：R575.2[医药卫生—消化系统]