摘要
目的 探讨miR-126在大鼠心肌缺血再灌注（I/R）早期的表达及抗凋亡作用.方法 48只SD大鼠随机分为假手术（Sham）、I/R 2 h、I/R 4 h、I/R 6 h组,每组12只大鼠,比较各组缺血区心肌细胞凋亡蛋白水平及miR-126表达水平.构建重组腺病毒rAAV9-ZsGreen-pre-miR-126载体,24只SD大鼠随机分为：①I/R组：大鼠转染空白病毒后I/R 2 h;②I/R＋miR-126组：大鼠转染rAAV9-ZsGreen-premiR-126后I/R 2 h,再次比较各组缺血区心肌细胞凋亡蛋白水平.结果 与Sham组相比,I/R 2 h、4h、6h组大鼠心肌缺血区miR-126表达进行性降低（P＜0.05）,非缺血区miR-126表达进行性升高（P＜0.05）;心肌凋亡蛋白BAX及CASPASE-3表达水平升高（P＜0.05）,抗凋亡蛋白BCL-2表达水平降低（P＜0.05）.与I/R组相比,I/R＋miR-126干预组心肌凋亡蛋白BAX及CASPASE-3表达水平明显减少,抗凋亡蛋白BCL-2表达水平增加（P＜0.05）.结论 在I/R早期大鼠心肌缺血区miR-126表达随再灌注时间延长进行性下降,并伴随心肌细胞凋亡进展;过表达miR-126可减少I/R导致的心肌细胞凋亡,发挥保护心功能的作用.
Objective To investigate the expression of microRNA-126 （miR-126） and its protective ef- fects in rat myocardium during early phase of ischemia-reperfusion. Methods 48 SD rats were randomly divided into Sham group（control group）, I/R 2 h group, I/R 4 h group, I/R 6 h group （ n=12 ）. To compare the expres- sion level of miR-126 and level of cell apoptosis between Sham group and the different I/R time point groups. rAAV9-ZsGreen-pre-miR-126 was successfully constructed and 24 SD rats were divided into two groups randomly （n=12）： （1）I/R group： rats were treated with I/R after transfected with rAAV9-ZsGreen by coronary injection. （2） I/R＋miR-126 group： rats were dealt with I/R after transfected with rAAV9-ZsGreen-pre-miR-126 by coronary injection. To compare again the expression level of miR-126 and level of cell apoptosis in the two groups. Results MiR-126 was down-regulated in the ischemic area after I/R compared with the Sham group at 2 h, 4 h and 6 h, but it was up-regulated in the non-ischemic area （P〈0.05）. The level of CASPASE-3 and BAX was in- creased in the I/R group than the Sham group at 2 h, 4 h and 6 h after I/R, but the level of BCL-2 was de- creased when compared with the Sham group. After tranfected with rAAV9-ZsGreen-pre-miR-126, the level of CASPASE-3 and BAX were decreased in I/R＋ miR-126 group by comparing with the I/R group, while the level of BCL-2 was increased when compared with the I/R group. Conclusion The expression of miR-126 was down- regulated and cell apoptosis was increased in ischemic area at the early phase of I/R. Over-expression of miR-126 can inhibit cell apoptosis and protect cardiac function.
出处
《中国心血管病研究》
CAS
2015年第11期1041-1046,1055,1056,共8页
Chinese Journal of Cardiovascular Research
