抗纤Ⅱ号对肝纤维化大鼠TGF-β1,Smad3表达的影响  

Effect of AntifibrosisⅡ on the expression of TGF-β1, Smad3 of hepatic fibrosis in rats

作　　者：李萍[1] 胡国龄[1] 谭德明[1] 刘国珍[1] 汪玲[1] 

机构地区：[1]中南大学湘雅医院传染病研究所,湖南长沙410008

出　　处：《中国现代医学杂志》2005年第13期1970-1973,共4页China Journal of Modern Medicine

摘　　要：目的在过去实践的基础上,欲探讨复方抗纤Ⅱ号抗肝纤维化的治疗机制。方法雄性Wistar大鼠分成5组,除正常对照外,余4组大鼠肝纤维化造模均采用腹腔注射猪血清(0.5mL/次,2次/周)。抗纤Ⅱ号早期治疗组在第3周给予中药灌胃,1g/100g每天1次。抗纤Ⅱ号晚期治疗组在造模第9周给予中药灌胃,1g/100g每天1次。γ-干扰素治疗组在造模第9周每天皮下注射10万单位的干扰素。模型组和正常对照组给等量的生理盐水灌胃。在12周杀大鼠,HE和Masson染色观察肝纤维化的形成,RT-PCR检测肝组织中TGF-β1和Smad3mRNA的表达,免疫组化观察TGF-β1和Smad3蛋白的表达。结果病理学观察,抗纤Ⅱ号早期治疗组显著逆转了猪血清诱导的肝纤维化,与模型组比较,经HE和Masson染色抗纤Ⅱ号治疗组能明显降解纤维化大鼠肝中的胶原(P<0.05)。PT-PCR分析TGF-β1和Smad3mRNA的表达在抗纤Ⅱ号治疗组均明显减少。同时分析表明TGF-β1和Smad3蛋白的表达在抗纤Ⅱ号治疗组均明显减少。结论抗纤Ⅱ号能逆转免疫引起的肝纤维化,这是由于能促进肝脏胶原的降解作用和抑制调节与纤维化有关的细胞因子TGF-β1及下游信号Smad3的表达,最终导致肝纤维化的逆转.肝纤维化的早期治疗用药优于后期的治疗。[Objective] On the basis of the clinical practice of treatment for hepatic fibrosis, We further explored and studied the mechanism of chinese herbal compound' Antifibrosis Ⅱ' in treating hepatic fibrosis. [Methods] Male wistar rats were divided into five groups .The rat fibrosis model was induced by pig serum, excepted for normal control group(group N),the other four groups were all given intraperitoneal injection of pig serum respectively (0.5 mL/once,2 times/week, total 12 weeks). In Antifibrosis Ⅱ early treatment group (group B), the rats were feed with Antifibrosis Ⅱby gavage, 1 g/100 g, once a day at the third week. In Antifibrosis Ⅱ late treatment group(group C) , the rats were fed with Antifibrosis Ⅱ by gavage, 1 g/100 g, once a day at the ninth week. Inγ-interferon treated group(group D), the rats were subcutaneous injected γ-interferon one hundred thousand every day at the ninth week .The model group(group A) and group N were fed with the same amount of saline by gavage. The rats were killed at the end of the twelfth weeks, the pathology of liver fibrosis was observed with HE stain and Masson stain. TGF-β1 mRNA and Smad3 mRNA, which is TGF-β1 downstream signal, were detected in liver samples with RT-PCR, immunohistochemical observe the expression of TGF-β1 and Smad3. [Results] Upon pathological examination, the Antifibrosis Ⅱ treatment had significantly reversed pig serum -induced liver fibrosis. In early treatment group B, the Antifibrosis Ⅱ could enhance the degradation of collagen in the rat's fibrotic liver according to HE and Masson staining compared with the fibrotic model group A (P <0.05). Moreover in Antifibrosis Ⅱ treatment group(B and C) the expression of TGF-β1 and Smad3 mRNA and its protein in liver was markedly reduced respectively according to RT-PCR analysis and immunohistochemistry as compared with group A. [Conclusion] The result showed that pig serum induced the rat's hepatic fibrosis can be obviously reversed by the Antifibrosis Ⅱtreatment. The mechanism of tre

关 键 词：肝纤维化 TGF—β1 SMAD3 

分 类 号：R575.2[医药卫生—消化系统]