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ID:34445268
大小:3.77 MB
页数:40页
时间:2019-03-06
《线粒体通透性转换孔在缺血预处理脑保护中的作用及机制》由会员上传分享,免费在线阅读,更多相关内容在学术论文-天天文库。
1、摘要目的:探讨线粒体通透性转换孔(mitochondrialpermeabilitytransitionpore,MPTP)在脑缺血再灌注损伤及缺血预处理脑保护中的作用。方法:将体外培养8天的海马神经元细胞分为五组,正常对照组(A组),缺血再灌注组(B组),缺血预处理+缺血再灌注组(C组),苍术苷+缺血再灌注组(D组),缺血预处理+苍术苷+缺血再灌注组(E组)。使用流式细胞术检测各组细胞凋亡率,罗丹明123染色流式细胞术检测线粒体膜电位,Western—blot检测Bcl一2,Bax的表达。结果:与A组比较,其余四组线
2、粒体膜电位均降低,神经元凋亡率升高(P<0.05);与B组比较,C组线粒体膜电位升高,神经元凋亡率升高,Bcl-2表达增加,Bax表达减少(P3、chondrialpermeabilitytransitionpore(MPTP)incerebralischemiareperfusionandischemiapreconditioningMethodsTheprimaryhippocampalneuroncellsofnewbornWistarratswereculturedfor8daysandrandomlydividedintofivegroups:controlgroup(A),ischemiareperfusiongroup(B),ischemiapre4、conditioninggroup+ischemiareperfusiongroup(C),atractyloside+ischemiareperfusiongroup(D)andhypoxicpreconditioninggroup+atractyloside+ischemiareperfusiongroup(E).Cellapoptosisratesineachgroupweremeasuredbyflowcytometry;Themitochondrialmembranepotentialwasdetectedb5、yflowcytometrythroughRhodamine123staining.WesternboltwasadoptedtoinvestigatetheexpressionofBcl一2andBaxResultsComparedwiththeothergroups,themitochondrialmembranepotentialofgroupAreducedandtheapoptosisrateincreasedsignificantly(P<0.05);ComparedtogroupB,themitochon6、drialmembranepotentialincreasedandtheapoptosisratedecreasedsignificantlyingroupC(P<0.05).TheexpressionofBcl-2increased(P<0.05),whileBaxdecreased(P<0.05).ComparedtogroupC,themitochondrialmembranepotentialdecreasedandtheapoptosisrateincreasedingroupE(P<0.05).Theex7、pressionofBcl一2decreased(P<0.05),whileBaxincreased(P<0.05)ConclusionIschemiapreconditioningdecreasestheapoptosisinducedbyischemiareperfusioninjuryinculturedhippocampalneuroncells,whichisrelatedtotheinhibitionofthemitochondrialpermeabilitytransitionpore.Keywords:8、Ischemiapreconditioning;Mitochondrialpermeabilitytransitionpore;Bcl.2/Bax目录弓I言一一一⋯⋯一一⋯一一一⋯一一一一~~⋯⋯一⋯1第——章实验试剂及仪器一一⋯⋯一一⋯⋯一一⋯⋯⋯一⋯⋯一21.1实验动彩刁一⋯⋯一一⋯⋯一一⋯⋯一一⋯⋯⋯⋯一⋯一一21.2材料与
3、chondrialpermeabilitytransitionpore(MPTP)incerebralischemiareperfusionandischemiapreconditioningMethodsTheprimaryhippocampalneuroncellsofnewbornWistarratswereculturedfor8daysandrandomlydividedintofivegroups:controlgroup(A),ischemiareperfusiongroup(B),ischemiapre
4、conditioninggroup+ischemiareperfusiongroup(C),atractyloside+ischemiareperfusiongroup(D)andhypoxicpreconditioninggroup+atractyloside+ischemiareperfusiongroup(E).Cellapoptosisratesineachgroupweremeasuredbyflowcytometry;Themitochondrialmembranepotentialwasdetectedb
5、yflowcytometrythroughRhodamine123staining.WesternboltwasadoptedtoinvestigatetheexpressionofBcl一2andBaxResultsComparedwiththeothergroups,themitochondrialmembranepotentialofgroupAreducedandtheapoptosisrateincreasedsignificantly(P<0.05);ComparedtogroupB,themitochon
6、drialmembranepotentialincreasedandtheapoptosisratedecreasedsignificantlyingroupC(P<0.05).TheexpressionofBcl-2increased(P<0.05),whileBaxdecreased(P<0.05).ComparedtogroupC,themitochondrialmembranepotentialdecreasedandtheapoptosisrateincreasedingroupE(P<0.05).Theex
7、pressionofBcl一2decreased(P<0.05),whileBaxincreased(P<0.05)ConclusionIschemiapreconditioningdecreasestheapoptosisinducedbyischemiareperfusioninjuryinculturedhippocampalneuroncells,whichisrelatedtotheinhibitionofthemitochondrialpermeabilitytransitionpore.Keywords:
8、Ischemiapreconditioning;Mitochondrialpermeabilitytransitionpore;Bcl.2/Bax目录弓I言一一一⋯⋯一一⋯一一一⋯一一一一~~⋯⋯一⋯1第——章实验试剂及仪器一一⋯⋯一一⋯⋯一一⋯⋯⋯一⋯⋯一21.1实验动彩刁一⋯⋯一一⋯⋯一一⋯⋯一一⋯⋯⋯⋯一⋯一一21.2材料与
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