Rab3A通过调控整合素亚单位α3的异常表达参与心肌细胞缺血/再灌注损伤的过程  

Rab3A is involved in myocardial ischemia/reperfusion injuryby regulating the aberrant expression of integrin subunitα3

作　　者：罗夏黎 涂艳虹 肖遥[2] LUO Xiali;TU Yanhong;XIAO Yao(Department of Integrative Medicine,Affiliated Hospital of Jianghan University Wuhan Sixth Hospital,Wuhan 430015,China)

机构地区：[1]江汉大学附属医院武汉市第六医院中西医结合科,湖北武汉430015 [2]湖北省中医院心内科,湖北武汉430000

出　　处：《陕西医学杂志》2025年第1期9-13,32,共6页Shaanxi Medical Journal

基　　金：国家自然科学基金资助面上项目(82026389);湖北省卫生健康委员会中医药科研项目(ZY2021M047)。

摘　　要：目的:探究G蛋白Rab3A和整合素亚单位α3(ITGA3)在心肌细胞缺血/再灌注损伤过程中的作用及潜在的可能分子机制。方法:采用缺氧/复氧法构建心肌细胞缺血/再灌注损伤模型,使用实时定量聚合酶链反应(RT-qPCR)和蛋白免疫印迹(Western blot)检测Rab3A在心肌细胞中的表达水平。细胞计数试剂盒-8(CCK-8)和细胞凋亡检测试剂盒评估Rab3A对心肌细胞活力和凋亡的影响;使用商用试剂盒检测Rab3A对心肌细胞氧化应激的影响。双荧光素酶实验用于验证Rab3A与ITGA3的结合。结果:缺氧/复氧诱导的心肌细胞中Rab3A mRNA和蛋白表达显著下调(均P<0.05)。过表达Rab3A逆转了缺血/再灌注损伤引起的心肌细胞活力下降和细胞凋亡水平上升(均P<0.05);过表达Rab3A能够抑制缺血/再灌注损伤引起的氧化应激(P<0.05)。Rab3A与ITGA3之间存在靶向结合位点,Rab3A可调控ITGA3的表达。结论:Rab3A可通过调控ITGA3的异常表达影响心肌细胞的增殖、凋亡及氧化应激状态,参与心肌细胞缺血/再灌注损伤过程。Objective:To investigate the role of G protein Rab3A and integrin subunitα3(ITGA3)in the process of myocardial ischemia/reperfusion injury and the potential molecular mechanism.Methods:The model of myocardial ischemia/reperfusion injury was established by hypoxia/reoxygenation method;The expression level of Rab3A in myocardial cells was detected by real-time quantitative polymerase chain reaction(RT-qPCR)and western blot.Cell counting kit-8(CCK-8)and apoptosis detection kits were used to assess the effects of Rab3A on cardiomyocyte viability and apoptosis,and the commercial kits were used to detect the effect of Rab3A on oxidative stress in cardiomyocytes.The dual luciferase assay was used to detect the binding of Rab3A to ITGA3.Results:The expression of Rab3A mRNA and protein in cardiomyocytes induced by hypoxia/reoxygenation was significantly down-regulated(P<0.05).Overexpression of Rab3A reversed the decrease in cell viability and increase in apoptosis level induced by ischemia/reperfusion injury(all P<0.05),as well as overexpression of Rab3A inhibited the oxidative stress induced by ischemia/reperfusion injury(P<0.05).There is a targeted binding site between Rab3A and ITGA3,and Rab3A can regulate the expression of ITGA3.Conclusion:Rab3A can affect the proliferation,apoptosis and oxidative stress of cardiomyocytes by regulating the abnormal expression of ITGA3,and participate in the process of myocardial ischemia/reperfusion injury.

关 键 词：RAB3A 整合素亚单位α3 心肌细胞 缺血/再灌注损伤 细胞凋亡 细胞活力 氧化应激 

分 类 号：R541[医药卫生—心血管疾病]