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《芪术颗粒对肝纤维化形成过程中磷脂酰肌醇-3-激酶/丝氨酸蛋白激酶信号传导通路的影响.pdf》由会员上传分享,免费在线阅读,更多相关内容在行业资料-天天文库。
1、·58·OhineseJournaIofInformationonTOMJuI.2014Vo1.21No.7芪术颗粒对肝纤维化形成过程中磷脂酰肌醇一3一激酶/丝氨酸蛋白激酶信号传导通路的影响刘绍能,杨清高,潘澎,陶夏平,刘慧敏中国中医科学院广安门医院,北京100053摘要:目的观察芪术颗粒在肝纤维化形成过程中对磷脂酰肌醇一3一激酶/丝氨酸蛋白激酶(PI3K/Akt)信号传导通路的影响,进一步阐明其抗肝纤维化的作用机制。方法将Wistar大鼠随机分为正常组、模型组、实验对照组和芪术颗粒组,采用四氯化碳复制肝纤维化模型,造模同日即给予相应治疗,芪术颗粒组2g
2、/(kg·d)灌胃,体积为i.0mL/100g体质量,实验对照组、模型组给予等体积无菌水,正常组正常喂养。分别于造模后第l、2、4周处理、取材,Westernblot免疫印迹法检测p-Akt(Ser473)、p-Akt(Thr308)、Bad(Ser136)、Caspase9蛋白表达。结果与正常组比较,模型组、芪术颗粒组各时间点pAkt(Ser473)、p-Akt(Thr308)、Bad(Ser136)、Caspase9蛋白表达均升高(P3、表达显著降低,差异有统计学意义(PO.05)。结论芪术颗粒对PI3K/Akt信号传导通路的激活有调控作用,从而抑制肝纤维化的发生和发展。关键词:芪术颗粒:磷脂酰肌醇一3一激酶/丝氯酸蛋白激酶;信号传导通路:大鼠D0I:10.3969/j.issn.1005—5304.2014.07.017中图分类号:R285.5文献标识码:A文章编号:1005—5304(2014)07—0058—04EffectsofQishuGranuleonPI3l4、ktSignalingTransductionPathwaysintheProcessofHepaticFibrosisLIUShao—neng,YANGQing.gao,PANPeng,TAOXia.ping,LIUHui.minrGuang’anmenHospitalofChinaAcademyofChineseMeScalSciences,Beijing100053,China)Abstract:ObjectiveToobservetheeffectsofQishugranuleonPI3K/Aktsignalingtransductionpath5、waysintheprocessofhepaticfibrosis,andfurtherexplaintheanti—hepaticfibrosismechanismofQishugranule.MethodsWistarratswererandomlydividedintonormalgroup,modelgroup,experimentalcontrolgroupandQishugranulegroup.LiverfibrosiswasduplicatedinratsbyintraperitonealinjectionofCC14,andtherat6、sweregivenappropriatetreatmentatthesameday.RatsinQishugranulegroupweregivenagavage2g/(kg·d),1.0mE/100g,whileratsinexperimentalcontrolgroupandnormalgroupweregiventhesameamountofaquaesterilisata.Ratsineachgroupweretakenlivertissuesamplesinthe1st,2ndand4thweek,andwerecheckedforthepr7、oteinexpressionlevelsofP—Akt(Ser473),P—Akt(Thr308),Bad(Serl36)andCaspase9byWesternblot.ResultsComparedwiththemodelgroup,expressionlevelsofP—Akt(Ser473),P—Akt(Thr308),Bad(Ser136)andCaspase9inmodelandQishugranulegroupsincreasedineverytimepoints(.P<0.05).Comparedwiththemodelgroup,ex8、pressionlevelofP—Akt(Ser473)inQishugranu
3、表达显著降低,差异有统计学意义(PO.05)。结论芪术颗粒对PI3K/Akt信号传导通路的激活有调控作用,从而抑制肝纤维化的发生和发展。关键词:芪术颗粒:磷脂酰肌醇一3一激酶/丝氯酸蛋白激酶;信号传导通路:大鼠D0I:10.3969/j.issn.1005—5304.2014.07.017中图分类号:R285.5文献标识码:A文章编号:1005—5304(2014)07—0058—04EffectsofQishuGranuleonPI3l
4、ktSignalingTransductionPathwaysintheProcessofHepaticFibrosisLIUShao—neng,YANGQing.gao,PANPeng,TAOXia.ping,LIUHui.minrGuang’anmenHospitalofChinaAcademyofChineseMeScalSciences,Beijing100053,China)Abstract:ObjectiveToobservetheeffectsofQishugranuleonPI3K/Aktsignalingtransductionpath
5、waysintheprocessofhepaticfibrosis,andfurtherexplaintheanti—hepaticfibrosismechanismofQishugranule.MethodsWistarratswererandomlydividedintonormalgroup,modelgroup,experimentalcontrolgroupandQishugranulegroup.LiverfibrosiswasduplicatedinratsbyintraperitonealinjectionofCC14,andtherat
6、sweregivenappropriatetreatmentatthesameday.RatsinQishugranulegroupweregivenagavage2g/(kg·d),1.0mE/100g,whileratsinexperimentalcontrolgroupandnormalgroupweregiventhesameamountofaquaesterilisata.Ratsineachgroupweretakenlivertissuesamplesinthe1st,2ndand4thweek,andwerecheckedforthepr
7、oteinexpressionlevelsofP—Akt(Ser473),P—Akt(Thr308),Bad(Serl36)andCaspase9byWesternblot.ResultsComparedwiththemodelgroup,expressionlevelsofP—Akt(Ser473),P—Akt(Thr308),Bad(Ser136)andCaspase9inmodelandQishugranulegroupsincreasedineverytimepoints(.P<0.05).Comparedwiththemodelgroup,ex
8、pressionlevelofP—Akt(Ser473)inQishugranu
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