piRNA-102526参与缺氧/复氧诱导心肌细胞焦亡作用及机制研究  

The Role and Mechanism of piRNA-102526 in Hypoxia/Reoxygenation-Induced Pyroptosis in Cardiomyocytes

作　　者：王少聪 鞠杰 陈鑫哲 于雪[1] 王昆[1] WANG Shao-cong;JU Jie;CHEN Xin-zhe;YU Xue;WANG Kun(Institute of Translational Medicine,Qingdao University,Qingdao 266021,China)

机构地区：[1]青岛大学转化医学研究院,青岛266021

出　　处：《青岛大学学报（自然科学版）》2023年第3期15-20,共6页Journal of Qingdao University(Natural Science Edition)

基　　金：国家自然科学基金(批准号:82070313)资助。

摘　　要：为探究piRNA-102526与心肌细胞焦亡的关系,体外构建小鼠乳鼠原代心肌细胞缺氧/复氧模型,设置3 h、6 h、9 h、12 h、24 h缺氧时间梯度及6 h复氧条件,检测小鼠乳鼠原代心肌细胞焦亡水平。利用qRT-PCR检测piRNA-102526表达水平,Western Blotting检测焦亡相关蛋白(GSDMD、Caspase-1、IL-1β、ASC)表达,PI染色和LDH活性检测细胞死亡。研究结果显示,小鼠乳鼠原代心肌细胞缺氧6 h/复氧6 h,细胞焦亡相关蛋白表达水平最高。抑制piRNA-102526表达,小鼠乳鼠原代心肌细胞焦亡加剧,过表达piRNA-102526,小鼠乳鼠原代心肌细胞焦亡减少。这表明,piRNA-102526能通过Caspase-1参与经典焦亡通路,调节小鼠乳鼠原代心肌细胞焦亡过程。The Hypoxia/Reoxygenation model of primary neonatal mouse cardiomyocytes was constructed in vitro to explore the relationship between piRNA-102526 and cardiomyocyte pyroptosis.The hypoxia time gradient of 3 h,6 h,9 h,12 h,24 h and the reoxygenation condition of 6 h were set to detect the degree of pyroptosis of primary neonatal mouse cardiomyocytes.The expression of piRNA-102526 was detected by qRT-PCR.Western Blotting was used to detect the expression of GSDMD,Caspase-1,IL-1βand ASC.PI staining and LDH were used to detect the degree of cell death.The results show that the expression level of pyroptosis-related proteins is the highest in primary neonatal mouse cardiomyocytes after hypoxia for 6 h and reoxygenation for 6 h.The expression of piRNA-102526 is inhibited,and the pyroptosis of primary neonatal mouse cardiomyocytes is aggravated.Overexpression of piRNA-102526,the pyroptosis of primary neonatal mouse cardiomyocytes is reduced.This shows that piRNA-102526 can regulate the pyroptosis process of primary neonatal mouse cardiomyocytes through the classical pyroptosis pathway involves in Caspase-1.

关 键 词：细胞焦亡 PIRNA 原代小鼠心肌细胞 心肌细胞损伤 GSDMD 

分 类 号：R542.2[医药卫生—心血管疾病]