远隔缺血预处理促进压力负荷性心肌肥厚术后逆重构的作用及机制研究  

Effect and mechanism of remote ischemic preconditioning on promoting reverse remodeling after pressure-loaded myocardial hypertrophy

作　　者：贾娜 裴汉军[1] JIA Na;PIE Hanjun(Department of Cardiology,the First Affiliated Hospital of Baotou Medical College,Inner Mongolia University of Science and Technology,Baotou 014010,China)

机构地区：[1]内蒙古科技大学包头医学院第一附属医院心内科,内蒙古包头014010

出　　处：《包头医学院学报》2023年第9期19-22,共4页Journal of Baotou Medical College

摘　　要：目的:研究远隔缺血预处理(remote ischemic preconditioning,RIPC)促进压力负荷性心肌肥厚(pressure-overload myocardial hypertrophy,POMH)术后逆重构的作用及机制。方法:建立H9C2心肌细胞模型,分为正常对照组(Sham)、POMH组、RIPC组,通过定量PCR与Western blot检测各组内细胞凋亡以及线粒体自噬相关蛋白的表达水平。结果:PCR结果显示,给予RIPC处理后能够明显抑制POMH中细胞凋亡率的升高;Western blot结果显示RIPC能够通过上调线粒体自噬相关蛋白表达达到促进POMH术后逆重构的作用。结论:RIPC能够促进POMH术后逆重构,其机制与线粒体自噬相关。Objective:To investigate the role and mechanisms of remote ischemic preconditioning(RIPC)in promoting the reverse remodeling after pressure-overload myocardial hypertrophy(POMH).Methods:H9C2 myocardial cell model was established.The rats were divided into the normal control group(Sham),POMH group and RIPC group.The apoptosis and expression levels of mitochondrial autophagy-related proteins in each group were detected by quantitative PCR and Western blot.Results:PCR results showed that RIPC could significantly inhibit the increasing rate of apoptosis in the POMH group.Western blot results showed that RIPC could promote reverse remodeling after POMH surgery by up-regulating the expression levels of mitochondrial autophagy-related proteins.Conclusion:RIPC could promote reverse remodeling after POMH surgery and its mechanism was related to mitochondrial autophagy.

关 键 词：远端缺血预处理 压力负荷性心肌肥厚 线粒体自噬 

分 类 号：R542.2[医药卫生—心血管疾病]