吡格列酮对游离脂肪酸介导的βTc细胞凋亡的干预作用.docxVIP

县人大常委会代表工作室XX年工作总结今年以来,结合保持共产】?目的研究吡格列酮对游离脂肪酸(FFA)诱导的小鼠胰岛βTc3细胞凋亡的影响及其作用机制。方法以βTc3细胞为研究对象颐,分为对照组及FFA组(,,mmol/L)。检测不同浓度FFA干预后βT玄c3细胞的增殖抑制率、细胞周期、细胞癜凋亡率;检测吡格列酮对FFA诱导的β独Tc3细胞凋亡的干预作用。结果FFA干预后的βTc3细胞增殖抑制率随FF┚A作用时间延长、浓度增加而进行性增加。各浓度FFA干预24h后βTc3细聂胞周期于G1/S检测点明显阻滞,凋亡谧细胞比例增加。吡格列酮干预FFA诱导蔹的βTc3细胞后24h,βTc3细胞脊周期阻滞减少,凋亡细胞比例明显减少。雠结论FFA水平异常不利于胰岛βTc3锃细胞生存,并可诱导βTc3细胞凋亡;曹吡格列酮有助于维护在FFA诱导下的胰整岛βTc3细胞的生存能力,并避免或减梭少其凋亡。【关键词】?噻唑烷二酮类脂肪酸类菲酯化胰岛糖尿病2型细胞凋亡ABSTRACT:?Objective?Toinvestigatethe⑼effectsofpioglitaz祯oneonFFAinducedap村optosisofβTc3cell,窳apancreaticβcelll叼ineinvitro.?Method椠s?βTc3wassubjectto隘differenttreatmentswithablankandthre↑ekindconcentration熘sofFFA,thatwere,an燥dmmol/LFFA.?TheMet趿hodofMTTwasusedtom愆easuretheprolifera婵tioninhibitionrate罱sforsuccessivethreedaysafterFFAinter攥vention.?Thechange误sofcellcyclewerede熹tected24hoursafter跪treatmentbyaflowcyぽtometry.?TUNELwasu栋sedtodeterminethea乏poptosisrateofcell噤s24hoursaftertreat俊ment.?TUNELandflow痞cytometrywereusedt押odetermineinterven蔹tioneffectofPiogli谱tazoneontheapoptosisofβTc3cellinduce⒑dbyFFA.?Results?In绀hibitionofβTc3wasi泫ncreasedwithprolon仅gedtreatmentofFFAa液ndincreasedFFAconcentrations.?Flowcy八tometryanalysissho箦wedthatcellcycleof惘βTc3celltreatedwit嬗hFFAofalltheconcen谯trationwasblockedi踩nphaseofG1/S.?Thep⑧ercentageofβTc3cel蛤lapoptosissubstant苡iallyincreasedduet擒oFFAtreatment.?Noo赦bviousabnormalchan墓geofcellcycleofβTc她3cellandasubstanti綮allydecreaseofperc人entageofapoptosisc哽ellsafterpioglitaz痫oneintervention.?C钪onclusion?Abnormal沙FFAlevelisextremel嗯yharmfulforsurviva楣lofβTc3cellculture力dinvitro,butpiogli驽tazonecouldmaintai票nthesurvivingabili哗tyofinsulinβTc3cel睾ldamagedbyFFA.KEYWORDS:?thiazolidin苷ediones;PPARgamma;愫fattyacids,noneste镶rified;diabetesmel鲆litus,type2;apopto缆sis福建医科大学学报?XX年7月④?第42卷第4期程惠希等：2型糖尿病跖是糖尿病的主要类型,但其发病机制尚未佝阐明。迄今的研究显示,胰岛β细胞功能仪缺陷和胰岛素抵抗是2型糖尿病主要病理┐生理基础,而游离脂肪酸(freefa蕖ttyacids,FFA)水平异常可能为重要的致病因素,长期暴露于高FF酚A可引起人和鼠胰岛β细胞脂质过载,细洳胞增殖下调和凋亡增加,胰岛素分泌减少[13]。过氧化物酶体增殖物激活皆受体(peroxisomeproli吣feratorsactivatorreceptorsgamma,