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时间:2020-06-03
《蕨麻正丁醇部位抑制缺氧损伤心肌细胞凋亡及Caspase3/9表达.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、第31卷第8期中华中医药学刊V0l_31NO.82013年8月CHINESEARCHIVESOFTRADITIONALCHlNESEMEDICINEAug.2013蕨麻正丁醇部位抑制缺氧损伤心肌细胞凋亡及Caspase3/9表达李灵芝,韦薇,龚海英,李建宇,郭鹏,张永亮,(1.武警后勤学院,天津300162;2.天津市职业与环境危害生物标志物重点实验室,天津300162)摘要:目的:研究蕨麻正丁醇部位对缺氧损伤心肌细胞凋亡及Caspase3、Caspase9表达的抑制作用。方法:建立大鼠原代培养心肌细胞缺氧模型,HE染色观察细胞组织形态,PI
2、—Hochesst3342染色观察细胞凋亡,RT—PCR技术及免疫细胞化学染色方法检测细胞Caspase3、Caspase9mRNA及其产物蛋白水平。结果:与模型组比较,正丁醇部位各剂量组Caspase3、Caspase9mRAN表达水平均显著降低(P<0.05或P<0.01);高剂量组Caspase3、Caspase9蛋白水平显著降低(P<0.01)。结论:蕨麻正丁醇部位可能通过减弱缺氧诱导的心肌细胞Caspase级联反应,抑制心肌细胞凋亡。关键词:蕨麻;缺氧;细胞凋亡中图分类号:R542.2文献标志码:A文章编号:1673—7717(20
3、13)08—1573—03EfectofN—butanolPotentillaAnserineL.FractiononExpressionsofCaspase3andCaspase9inCardiomyocyteInjuredbyHypoxiaLILingzhi,WEIWei,GONGHaiying,LIJianyu,GUOPeng,ZHANGYongliang,(1.LogisticalUniversityofChinesePeoplegArmedPoliceForces,Tianjin300162,China;2.TianjinKeyLa
4、boratoryofOccupationalandEnvironmentalHazardsBiomarkers,Tianjin300162,China)Abstract:Objective:Tostudytheinhibtingeffectofthen—butanolPotentillaanserineL.fractionontheapoptosisandtheexpressionsofCaspase3andCaspase9ofcardiomyocyteinjuredbyhypoxia.Methods:Todevelopamodelofcar
5、diomycyteinjuredbyhypoxiainratsinvitro.ThepathologychangesandtheapoptosisofcardiomycyteswereobservedseparatelybyHEstainingandPI—Hoechst3342.TheexpressionlevelsofCaspase3andCaspase9mRNAsinthecardio—mycyteswerestudiedbyreversetranscriptionpolymerasechainreaction(RT—PCR).Thelo
6、calizationsandlevelsoftheirproductproteinsinthecardiomycyteswereinvestigatedbyimmunocytochemistrystain.Rersult:Comparingwithmodelgroup,thepathologychangeswereimprovedbythen—butanolPotentillaanserineL.fractionandthenumberofapoptoticcardiomycyteswasreduced.Aftertreatedwithdif
7、ferentdosesofn—butanolPotentillaanserineL.fraction,theexpres—sionlevelsofCaspase3andCaspase9mRANsincardiomyocytessignificantlydecreased(P<0.05orP<0.01).Thecontentsoftheirproductproteinssignificantlydecresedinthehighdosegroup(P<0.01).Conclusion:Then—butanolPotentillaanserine
8、L.fractionexertsaremarkablyinhibitingeffectoncardiomyocyteduringhypoxiaandthismayb
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