中国现代医生2019，Vol.57Issue(10)：38-41,4.
Notch信号通路经ROCK2对缺氧/复氧诱导H9c2心肌细胞凋亡的影响
Effect of Notch signaling pathway on apoptosis of H9c2 cardiomyocytes induced by hypoxia/reoxygenation by ROCK2
摘要
Abstract
Objective To investigate the effect of Notch signaling pathway on the apoptosis of H9 c2 cardiomyocytes induced by hypoxia/reoxygenation in rat cardiomyocytes via ROCK2. Methods A total of 180 SD neonatal rats were selected as the study materials and divided into 6 groups. The expression of Hes1, myocardial cell viability, release of cardiomyocyte lactate dehydrogenase, cardiomyocyte apoptosis and NICD, Bcl2, Caspase3 and Hes1 expression levels were detected. Results The OD value of SI/R group was significantly lower than that of the control group (P<0.05), the OD value of Jagged1+ SI/R group was significantly different from that of the SI/R group and the control group (P<0.05).There was significant difference in the OD value between Jagged+DAPT+SI/R group and the Jagged1+SI/R group (P<0.05). There was no significant difference in the OD value between the control group and Jagged1 group, the DAPT group (P>0.05). The LDH release rate and apoptosis rate of SI/R group, Jagged1+SI/R group and Jagged +DAPT+SI/R group were significantly higher than those of the control group (P<0.05). The levels of Notch1, Hes1 and Bcl2 in the SI/R group, Jagged1+SI/R group and Jagged+DAPT+SI/R group were significantly decreased, while the expression of Caspase3 was significantly increased (P<0.05). Conclusion Notch signaling pathway plays an important role in the regulation of myocardial ischemia/reperfusion, and has an important effect on the induction of H9 c2 cardiomyocyte apoptosis.Activation of Notch signaling pathway can inhibit ischemia/reperfusion injury.关键词
Notch信号通路/ROCK2/心肌缺血/再灌注/H9c2心肌细胞凋亡Key words
Notch signaling pathway/ROCK2/Myocardial ischemia/reperfusion/H9c2 cardiomyocyte apoptosis分类
医药卫生引用本文复制引用
易松,杨丹,幸志强..Notch信号通路经ROCK2对缺氧/复氧诱导H9c2心肌细胞凋亡的影响[J].中国现代医生,2019,57(10):38-41,4.基金项目
江西省宜春市科技局重点计划课题项目(JXYC2014KSA001) （JXYC2014KSA001）
