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ID:31080909
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页数:11页
时间:2019-01-06
《染料木黄酮对叔丁基过氧化氢诱导的内皮细胞凋亡的抑制作用》由会员上传分享,免费在线阅读,更多相关内容在工程资料-天天文库。
1、染料木黄酮对叔丁基过氧化氢诱导的内皮细胞凋亡的抑制作用王凡*,张婷*,糜漫天(400038重庆,第三军医大学军事预防医学院营养与食品卫生学教研室,重庆市医学营养研究中心,重庆市营养与食品安全重点实验室)[摘要]目的研究染料木黄酮(Genistein,Gen)对叔丁基过氧化氢(tert-butylhydroperoxide,t-BHP)诱导的人血管内皮细胞株EA.hy926凋亡的保护效应并探索相关分子机制。方法以t-BHP建立氧化应激损伤体外模型,CCK-8法、流式细胞仪检测Gen对内皮细胞活力、凋亡的影响,Westernblotting法检测Gen对内皮细
2、胞caspase-3表达的影响和PPARγ蛋白表达的影响,免疫细胞化学法检测Gen对细胞PPARγ表达定位。结果t-BHP能明显抑制EA.hy926生长,半数抑制浓度(IC50)约为100μmol/LM(问题1:请全文修改);Gen(5nM~500nmol/LM)能显著抑制t-BHP诱导的内皮细胞凋亡,并呈明显的剂量-效应关系;Gen能够显著激活PPARγ蛋白的表达,并诱导其核易位。结论Gen抑制t-BHP诱导的内皮细胞的凋亡可能与PPARγ的活化有关。(问题2:结论中未涉及“保护效应”,与“目的”未对应。)[关键词]染料木黄酮叔丁基过氧化氢PPARγ[中
3、图法分类号][文献标志码]Thedepressingeffectofgenisteinonapoptosisinducedbytert-butylhydroperoxideinhumanvascularendothelialcellWangFan,ZhangTing,MiMantian(DepartmentofNutritionandFoodHygiene,ChongqingKeyLaboratoryofNutritionandFoodSafety,ChongqingMedicalNutritionResearchCenter,CollegeofMilit
4、aryPreventiveMedicine,ThirdMilitaryMedicalUniversity,Chongqing,400038,China)Abstract:ObjectiveTostudytheprotectioneffectsofgenisteinattenuatestheEA.hy926celllineapoptosisinducedbytert-butylhydroperoxide(t-BHP)anditsmechanismsofactivatingperoxisomeproliferators-activatedreceptorgam
5、ma(PPARγ).MethodsAninvitromodelofoxidativestressbyinducedbyt-BHPwasestablished.CCK-8assaywasusedtodetecttheeffectofgenisteinontheproliferationofEA.hy926celllineunderoxidativestress.FlowcytometerwasusedtodetecttheeffectofgenisteinontheapoptosisofEA.hy926celllineunderoxidativestress
6、.Immunohistochemistrywasusedtoanalyzethenuclear-translocationofPPARγactivatedbygenistein.WeternblottingwasusedtodetecttheexpressofActived-Caspase-3p17andPPARγproteinbygenistein.Resultst-BHPcaninducetheapoptosisofEA.hy926celllineobviouslyandIC50wasabout100μM.Genisteincansignificant
7、lyrepresstheEA.hy926celllineapoptosisinducedbyt-BHPrangefrom5nMto500nMbydose-effectrelationship.Genisteincaneffectivelyinducethenuclear-translocationofPPARγandactivateitsproteinexpressionConclusionGenisteincanrepresstheEA.hy926celllineapoptosisinducedbyt-BHPpossiblelybymechanismof
8、activatingPPARγ.KeyWords:genistei
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