吡格列酮预处理对大鼠缺血-再灌注心肌细胞凋亡及线粒体atp敏感性钾通道的影响论文

《吡格列酮预处理对大鼠缺血-再灌注心肌细胞凋亡及线粒体atp敏感性钾通道的影响论文》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、吡格列酮预处理对大鼠缺血/再灌注心肌细胞凋亡及线粒体ATP敏感性钾通道的影响论文李健,冯义柏,田莉,郎明健,杨汉东【摘要】目的:观察吡格列酮(Pio)对在体大鼠心肌缺血/再灌注心肌细胞凋亡及线粒体ATP敏感性钾通道影响，探讨Pio对心肌缺血损伤保护作用及其机制.方法:24只SD大鼠随机分为假手术组（SO组）,缺血/再灌注组（I/R组），Pio预处理组（Pio组）和线粒体ATP敏感性钾通道阻滞剂5羟基葵酸（5HD）+Pio组（5HD+Pio组）4组.各组于缺血/再灌注前24h尾静脉注射相应溶媒及药物，5HD+Pio组注入5HD10mg/kg30min后再给予Pio3

2、mg/kg；Pio组只注入Pio3mg/kg；SO组不结扎前降支，4h后取出心脏；余三组结扎前降支30min，再灌注4h后取出心脏.用透射电镜观察心肌线粒体超微结构的改变；采用TUNEL法和免疫组化法检测缺血心肌细胞凋亡和Bcl2，Bax，Caspase3蛋白的表达以及RTPCR法测FasmRNA的表达.又另取18只SD大鼠随机分成SO.freelRNA的表达水平.I/R组与5HD+Pio组相比,差异无统计学意义(P0.05).结论：Pio预处理可通过保护心肌线粒体结构，减少心肌细胞凋亡及梗死范围,保护缺血心肌损伤作用可被线粒体ATP敏感性钾通道阻滞剂所对抗.【关键

3、词】吡格列酮；缺血再灌注；凋亡；线粒体；钾通道【Abstract】AIM:Toobservetheeffectsofpioglitazoneonmyocardialapoptosisinducedbymyocardialischemia/reperfusion(I/R)injuryandmitochondriaATPsensitivepotassiumchannelinratsinvivoandtoexplorethemechanismofpioglitazoneprotectionfrommyocardialI/Rinjury.METHODS:Tlydividedint

4、o4groups:shamoperatedgroup,I/Rgroup,pioglitazonetreatmentgroupand5hydroxydecanoicacid(5HD)+pioglitazonegroup.Apartfromtheshamoperatedgroup,I/R,pioglitazoneand5HD+pioglitazonegroupsinisteredsolventordrugsintravenously24hbeforeocclusion,.freelg/kg)and5HD(10mg/kg)pluspioglitazone(3mg/kg

5、).In5HDpioglitazonegroup,5HDinbeforepioglitazoneinjection.TheshamoperatedgroupininI/R,pioglitazoneand5HD+pioglitazonegroups.ThentheleftanteriordescendingbranchovedtobeusedforobservingtheultrastructureofmitochondriaandmeasuringtheapoptosisratebyTUNELanddetectingtheexpressionsofBcl2,Ba

6、x,Caspase3proteinsmunohistochemistryandFasmRNAlydividedinto3groups:shamoperatedgroup,I/Rgroup,pioglitazonetreatmentgroupandthesizeofmyocardialinfarctionageofmitochondrialultrastructureinpioglitazonegroupoperatedgroup,theapoptosisandpositivecellindex(PCI)ofBcl2,Bax,Caspase3proteinsandt

7、helevelofFasmRNAinI/R,pioglitazoneand5HD+pioglitazonegroupsRNAinpioglitazonegroupI/Rinjurybyimprovingmitochondrialultrastructureandreducinginfarctsize,andbydecreasingapoptosis.ThecardioprotectiveeffectscanbeinhibitedbyblockerofmitochondrialATPsensitivepotas