欢迎来到天天文库
浏览记录
ID:56135653
大小:665.57 KB
页数:5页
时间:2020-06-04
《白藜芦醇预先干预对血管紧张素Ⅱ诱导小鼠足细胞内质网应激性凋亡的影响.pdf》由会员上传分享,免费在线阅读,更多相关内容在应用文档-天天文库。
1、中华糖尿病杂志2014年8月第6卷第8期ChinJDiabetesMellitus,August2014,Vo1.10.8·589·.论著.白藜芦醇预先干预对血管紧张素Ⅱ诱导小鼠足细胞内质网应激性凋亡的影响秦洁张姬欣马春明聂琳张红霞马禅娟柳洁【摘要】目的研究内质网应激及c.Jun氨基末端激酶(JNK)通路在血管紧张素II(AngⅡ)所致肾小球足细胞损伤中的作用及白藜芦醇对其的保护机制。方法小鼠足细胞诱导分化,随机分为对照组(C组)、高AngII组、白藜芦醇干预(AngII+Res)组、JNK通路特异抑制剂SP600125干预组,对照组采用RPMI1640培养
2、,AngI1浓度为10~mol/L,白藜芦醇浓度为20~mol/L,SP600125浓度为20p.molIL。作用48h后,倒置显微镜下观察各组足细胞形态,并用流式细胞仪测定细胞凋亡率,实时定量聚合酶链反应(PCR)和Westernblotting法分别测定葡萄糖调节蛋白78(GRP78)和磷酸化JNK(p.JNK)mRNA及蛋白的表达。各组间数据比较采用t检验。结果与对照组相比,AngⅡ组细胞凋亡率升高,GRP78mRNA、P.JNKmRNA的表达增多(t=9.318、6.063、7.160,均P<0.05),且GRP78蛋白、p-JNK蛋白的表达也上调(
3、GRP78蛋白和p-JNK蛋白I、Ⅱ条带t=4.116、5.085、5.117,均P<0.05)。与AnglI组相比,AngII+Res干预组足细胞凋亡率降低,GRP78mRNA、蛋白表达减少(t=14.328、4.530、3.977,均P<0.05),P.JNKmRNA、p-JNK蛋白的表达亦减少(mRNA和蛋白I、Ⅱ条带t=4.590、4.990、4.991,均P<0.05)。与AngII组相比,SP600125干预组足细胞凋亡率降低(=10.756,P<0.05),p-JNKmRNA、蛋白的表达亦减少(mRNA和蛋白I、Ⅱ条带t=5.408、4.901
4、、4.886,均P5、a,MaChanjuan,LiuJie.DepartmentofEndocrinology,ShanxiProvincialPeoplesHospital,Taiyuan030012,ChinaCorrespondingauthor:LiuJie,Emaihliufie6@medmail.com.elt【Abstract]ObjectiveTostudytheroleofendoplasmicreticulumstressandc-JunN—terminalkinase(JNK)pathwayinangiotensinI/(AngⅡ)-causedglome6、rularpodocyteinjuryandtheprotectionmechanismofresveratro1.MethodsThemousepotocyteswereinduceddifierentiationandrandomlydividedintocontrolgroup,highAngⅡgroupandresveratrolinterventiongroup(AngII+Resgroup),andthespecificinhibitorofJNKpathwaySP600125interventiongroupfAngⅡ+SP600125grou7、p).ControlgroupwasincubatedwithRPM11640medium,theAngI/concentrationwas10~mol/L,resveratrolconcentrationwas20p,mol/L,SP600125concentrationwas20p,mol/L.Podocytemorphologyindifferentgroupswasobservedwithinvertedmicroscopeaftertreatedfor48hours,andtheapoptosisratewasmeasuredwithflowcyt8、ometer.ThemRNAandproteinex
5、a,MaChanjuan,LiuJie.DepartmentofEndocrinology,ShanxiProvincialPeoplesHospital,Taiyuan030012,ChinaCorrespondingauthor:LiuJie,Emaihliufie6@medmail.com.elt【Abstract]ObjectiveTostudytheroleofendoplasmicreticulumstressandc-JunN—terminalkinase(JNK)pathwayinangiotensinI/(AngⅡ)-causedglome
6、rularpodocyteinjuryandtheprotectionmechanismofresveratro1.MethodsThemousepotocyteswereinduceddifierentiationandrandomlydividedintocontrolgroup,highAngⅡgroupandresveratrolinterventiongroup(AngII+Resgroup),andthespecificinhibitorofJNKpathwaySP600125interventiongroupfAngⅡ+SP600125grou
7、p).ControlgroupwasincubatedwithRPM11640medium,theAngI/concentrationwas10~mol/L,resveratrolconcentrationwas20p,mol/L,SP600125concentrationwas20p,mol/L.Podocytemorphologyindifferentgroupswasobservedwithinvertedmicroscopeaftertreatedfor48hours,andtheapoptosisratewasmeasuredwithflowcyt
8、ometer.ThemRNAandproteinex
此文档下载收益归作者所有