硫喷妥钠调控miR-664-1-5p对氯化钴诱导的心肌细胞缺氧损伤的保护作用  

Protective effect of sodium thiopental on cobalt chloride-induced cardiomyocyte hypoxia injury by regulating miR-664-1-5p

作　　者：许明星[1] 郑传东[1] 杨鹏[2] 杨娜[1] XU Mingxing;ZHENG Chuandong;YANG Peng;YANG Na(Department of Anesthesiology, The Third People's Hospital of Chengdu, Chengdu 610031, China;Department of Pathology, The Third People's Hospital of Chengdu, Chengdu 610031, China)

机构地区：[1]成都市第三人民医院麻醉科,四川成都610031 [2]成都市第三人民医院病理科,四川成都610031

出　　处：《西部医学》2021年第3期342-346,351,共6页Medical Journal of West China

基　　金：成都市卫计委科研课题(2015077)。

摘　　要：目的研究硫喷妥钠对氯化钴(CoCl_(2))诱导的大鼠心肌细胞H9c2缺氧损伤的保护作用及潜在机制。方法对H9c2细胞进行CoCl_(2)处理建立缺氧损伤模型(模型组),分别采用125、250、500 nmol/L的硫喷妥钠处理600μmol/L CoCl_(2)的DMEM培养液培养H9c2细胞,分别记为药物1、2、3组,对照组为不含CoCl_(2)的DMEM培养液培养H9c2细胞。CCK8法和流式细胞术分别检测细胞存活率和凋亡率,Western blot测定P21和Caspase-3蛋白水平,分光光度法测定H9c2细胞中丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性,qRT-PCR检测CoCl_(2)诱导后H9c2细胞miR-664-1-5p的表达水平。结果与对照组相比,模型组心肌细胞H9c2中MDA、P21和Caspase-3含量升高,细胞存活率降低,凋亡率升高,miR-664-1-5p含量和SOD活性均降低,差异均具有统计学意义(均P<0.05);与模型组相比,药物2组和药物3组H9c2细胞中MDA、P21和Caspase-3含量降低,细胞存活率升高,凋亡率降低,miR-664-1-5p含量和SOD活性均上升,差异均具有统计学意义(均P<0.05);过表达miR-6641-5p可抑制CoCl_(2)诱导的H9c2细胞凋亡,提高细胞存活率;抑制miR-664-1-5p能减弱硫喷妥钠对CoCl_(2)诱导的心肌细胞缺氧损伤的保护作用。结论硫喷妥钠通过miR-664-1-5p提高CoCl_(2)诱导的大鼠心肌细胞H9c2存活率,抑制细胞凋亡,减轻细胞损伤。Objective To investigate the protective effects of sodium thiopental on injury of rat cardiomyocyte H9c2 induced by cobalt chloride(CoCl_(2))and its potential mechanism.Methods H9c2 cells were treated with CoCl_(2) to establish an hypoxic injury model,and then the model group was treated with 125 nmol/L,250 nmol/L,500 nmol/L sodium thiopental(drugs 1,2,and 3 groups).The cell survival rate and apoptosis rate were detected by CCK8 assay and flow cytometry,respectively.The expression levels of P21 and Caspase-3 proteins were determined by Western blot.The content of malondialdehyde(MDA)and the activity of superoxide dismutase(SOD)in H9c2 cells were determined by spectrophotometry,and the level of miR-664-1-5p in H9c2 cells induced by CoCl_(2) was detected by qRT-PCR.Results Compared with the control group,the levels of MDA,P21 and Caspase-3 in model group increased significantly,the cell survival rate decreased,the apoptosis rate increased,the level of miR-664-1-5p and the activity of SOD decreased.Compared with the model group,the levels of MDA,P21 and Caspase-3 in group+drug 2 and 3 significantly decreased,the cell survival rate increased,while the apoptosis rate reduced,and the levels of miR-664-1-5p and SOD activity increased.Over-expression of miR-664-1-5p inhibited the apoptosis of H9c2 cells induced by CoCl_(2) and improved the survival rate of cells.Inhibition of miR-664-1-5p attenuates the protective effect of sodium thiopental on the hypoxia injury of cardiomyocytes H9c2 cells induced by CoCl_(2).Conclusion Sodium thiopental improves the survival rate,inhibits cell apoptosis and alleviates cell injury of rat cardiomyocytes H9c2 induced by CoCl_(2) through regulating miR-664-1-5p.

关 键 词：硫喷妥钠 心肌细胞 H9C2 氯化钴 miR-664-1-5p 存活率 凋亡 

分 类 号：R329.28[医药卫生—人体解剖和组织胚胎学]