摘要
【目的】探讨通过腺病毒转染过氧化物酶体增殖物激活受体71（PPARTl）基因对大鼠心肌缺血=再灌注后肌钙蛋白I（cTnI）浓度、凋亡指数（AI）、凋亡通道蛋白caspase-3和caspase-9的影响。【方法130只SD大鼠随机分为三组（n=10）：假手术组（Sham组）、心肌缺血一再灌注损伤组（MIRI组）、过表达PPARTI组（PPAR71组）。Sham组和MIRI组经冠脉转染携带绿色荧光蛋白的腺病毒载体（Ad-EGFP）至心肌组织，PPARyl组转染携带PPAR71基因的腺病毒载体（Ad—PPARyl）。稳定3d后，各组建立心肌缺血-再灌注损伤模型（或假实验），缺血30rain，再灌注120min，检测cTnI含量、心肌组织AI、caspase-3和caspase-9表达情况。【结果】再灌注末，MIRI组和PPARTl组cTnl含量、心肌组织A1、caspase-3和caspase-9表达明显高于Sham组（P〈O．05），PPAR71组低于MIRI组（P〈0．05）。【结论】大鼠心肌过表达PPAR71基因能够改善心肌缺血一再灌注损伤，抑制凋亡，并且是通过抑制caspase-3和caspase-9的表达上调而实现。
[Objective]To explore the influence of adenovirus transfected with peroxisome proliferator-acti- vated receptor-gamma 1 （PPAR71） gene on troponin I（cTnI）, apoptosis index（AI） and apoptosis channel pro- teins caspase-3 and caspase-9 after rat myocardial ischemia-reperfusion. [Methods]Thirty SD rats were ran- domly divided into sham operation group（Sham group）, myocardial ischemia-reperfusion injury group（MIRI group） and PPARγ1 gene overexpression group（PPARγ1 group） with 10 in each. Myocardial tissues were transfected with recombinant adenovirus vector mediated enhanced green fluorescent protein （Ad-EGFP） via coronary artery in Sham group and MIRI group, while myocardial tissues were transfected with recombinant adenovirus vector mediated human PPARγ1 gene（Ad-PPARγ1） in PPARyl group. Myocardial ischemia reper- fusion injury model（or sham operation） in each group was established three days later. The content of cTnI, AI of cardiac tissue and the expression of caspase-3 and caspase-9 were detected at 30min after isehemia and 120min after reperfusion. [Results]At the end of reperfusion, the content of cTnI, AI of cardiac tissue and the expression of caspase-3 and caspase-9 in MIRI group and PPARy1 group were obviously higher than those in Sham group（ P 〈0.05）, and those in PPARγ1 group were lower than those in MIRI group（ P 〈0. 05）. [Conclusion]Overexpression of PPARγ1 gene in rat myocardial tissue can improve myocardial ischemia-reper- fusion injury and inhibit apoptosis through inhibiting the up-regulation of the expression of caspase-3 and caspase-9.
出处
《医学临床研究》
CAS
2013年第7期1369-1371,共3页
Journal of Clinical Research
关键词
心肌缺血
心肌再灌注损伤
基因
细胞凋亡
Myocardial Ischemia
Myocardial Reperfusion Injury
Genes
Apoptosis
