l4诱导的肝纤维化大鼠TGF.docx

l4诱导的肝纤维化大鼠TGF
编辑。【摘要】 [目的]l4诱导的大鼠肝纤维化肝脏TGF-1及Smad3,Smad7表达的影响,探讨其抗纤维化的作用机制。[方法]Wistar大鼠40只,随机分成正常对照组,模型对照组,软肝饮治疗组,鳖甲软肝片对照组,l4背部皮下注射构建肝纤维化模型,行HE和VG染色,光镜下观察肝组织肝纤维化程度。同时免疫组化SABC方法检测胂各组TGF-1、Smad3和Smad芹7的表达。[结果]与正常对照组相比,模型组TGF-1、Smad3表达明显搁增强,Smad7表达明显下降。经软肝ゃ饮治疗后大鼠肝脏TGF-1表达比模型组减弱。软肝饮同时下调Smad3的表侨达,上调Smad7的表达。另外,软肝殍饮组大鼠肝脏病理变化显著改善。[结论摺]肝炎平对大鼠肝纤维化肝脏TGF-1む/Smad信号通路有明显的影响,能抑制CCl4诱导的大鼠肝纤维化,其作用{机制可能为抑制TGF-1表达,下调S迪mad3及上调Smad7的表达。
【关键词】 软肝饮;TGF-1/Smad信号通路;肝纤维化
Abstrac妙t:[Aim]Tostudythee扶ffectsofRuanganyin篁onTGF-1,Smad3,Smad大7expressionsofthee廾xperimentalhepatic哇fibrosisinducedbyc挠
l4)inrats,andto币exploreitsanti-fib┆roticmolecularmech庵anism.[Method]Fort哽yhealthyWistarrats悴wererandomlydivide妯dintonormalcontrol孵group,l4-induce床dhepaticfibrosisgr孢oup,andRuanganyint┎alinebyintragastri乩calirrigation,andtheothergroupsweres≌ubcutaneousinjectel4toestabli肿shhepaticfibrosish禹istologicalchanges爻ofthelivertissuesw郓ereexaminedbypathologicalprotEinexpr蟹essionoftransformi屯nggrowthfactorbeta癌1(TGF-1)andSmad3,S督mad7weremeasuredby站immunohistochemica铅ltechnique.[Result脲]parisonwitht倚hoseinmodelgroup,t彦helevelsofTGF-1wer赓esignificantlydecreasedaftertreatmentwith,thelevelsofS桶mad3wasalsodown-,th阕elevelofSmad7expreョssionwassignifican皇tlypathologicalchaんngesoflivertissuesinRuanganyingroups满werealsomarkedlyal讲leviated.[Conclus