论文部分内容阅读
目的研究长链非编码RNA HIF1A-AS1对大鼠缺血再灌注损伤的调控作用,并初步探索其机制。方法构建大鼠心肌缺血再灌注损伤和心肌细胞缺氧/复氧损伤模型,利用实时定量PCR检测HIF1A-AS1的表达。采用siRNA抑制心肌细胞HIF1A-AS1的表达并制备缺氧/复氧损伤模型,用MTT法检测心肌细胞生长活力,ELISA法检测培养液中乳酸脱氢酶的水平,蛋白质印迹法检测自噬相关蛋白Beclin-1的表达变化。结果 HIF1A-AS1在缺血再灌注大鼠心肌组织和缺氧/复氧损伤心肌细胞中表达上调。抑制HIF1A-AS1表达可保护心肌细胞,逆转缺氧/复氧刺激导致的心肌细胞生长活力降低、乳酸脱氢酶分泌水平增高、自噬标志蛋白Beclin-1表达增高现象。结论抑制长链非编码RNA HIF1A-AS1,可能通过抑制心肌细胞的过度自噬抵抗缺血再灌注诱导的心肌损伤。
Objective To study the regulatory effect of long-chain non-coding RNA HIF1A-AS1 on ischemia-reperfusion injury in rats and its mechanism. Methods Myocardial ischemia-reperfusion injury and myocardial hypoxia / reoxygenation injury model were established. The expression of HIF1A-AS1 was detected by real-time quantitative PCR. The siRNA was used to inhibit the expression of HIF1A-AS1 in cardiomyocytes and the hypoxia / reoxygenation injury model was established. The viability of cardiomyocytes was assayed by MTT assay. The level of lactate dehydrogenase in culture solution was detected by ELISA. The expression of autophagy-related protein Beclin-1 expression changes. Results The expression of HIF1A-AS1 was up-regulated in myocardium and hypoxia / reoxygenation injured myocytes in ischemia-reperfusion rats. Inhibition of HIF1A-AS1 expression can protect cardiomyocytes, reversal of hypoxia / reoxygenation induced myocardial cell viability decreased, increased secretion of lactate dehydrogenase, autophagy protein Beclin-1 expression increased phenomenon. Conclusion Inhibition of long-chain non-coding RNA HIF1A-AS1 may protect myocardium from ischemia-reperfusion-induced myocardial injury by inhibiting excessive autophagy in cardiomyocytes.