高糖调节c-Src/PI3K/ERK通路诱导心肌H9c2细胞凋亡  

Hyperglycemia Induces Cardiac Cell Apoptosis Via Regulating c-Src/PI3K/ERK Pathway

作　　者：武倩 李文静 贺辉 颜洪竹 甘亚平 刘复兴 宁志丰 鲍翠玉 WU Qian;NING Zhi-feng;BAO Cui-yu(School of Nursing, Hubei University of Science and Technology ,Xianning Hubei 431100, China)

机构地区：[1]湖北科技学院护理学院,湖北咸宁437100 [2]湖北科技学院基础医学院

出　　处：《湖北科技学院学报（医学版）》2019年第2期110-113,117,共5页Journal of Hubei University of Science and Technology(Medical Sciences)

基　　金：湖北省自然科学基金项目(2015CFC773);湖北科技学院糖尿病专项(ZX1004和ZX1315);湖北科技学院临床医学专项(LCZX201503和LCZX201518);咸宁市科技计划项目(44)

摘　　要：目的明确高糖环境对大鼠心肌细胞H9c2的损伤作用及其作用机制。方法常规培养大鼠心肌细胞H9c2,设立正常糖浓度组(5.5mmol/L)、高糖组1(30mmol/L)、高糖组2(60mmol/L),与H9c2孵育一定时间后,MTT法检测细胞增殖情况,β-半乳糖苷酶染色法检测衰老,Hoechst 33342/PI双染法检测凋亡,自噬检测试剂盒法检测自噬,Western blot检测相关信号通路的变化。结果在高糖环境中,H9c2的增殖能力受损,并呈剂量依赖性;孵育4h后,H9c2细胞出现显著凋亡,但是没有出现显著衰老和自噬现象。在机制研究中,发现共孵育4h后,c-Src和PI3K表达减少,磷酸化的ERK表达增加,总的ERK表达没有变化。结论高糖环境中大鼠心肌细胞H9c2增殖受损,凋亡增加,其作用机制与信号通路c-Src/PI3K/ERK表达失调有关。Objective To study the effect of high glucose on cardiac cells and its mechanism. Methods Rat heart-derived H9 c2 cells were cultured in DMEM medium supplemented with 100 U/ml penicillin and 100μg/ml streptomycin.After incubation with different concentrations of glucose(5.5 mmol/L,30 mmol/L,60 mmol/L),MTT method was applied to detect the proliferation ability,β-gal staining and Hoechst 33342/PI double staining were performed to test cell senescence and apoptosis,respectively,and western blot was adopted to measured the expression of signaling pathway proteins.In addition,autophagic activity was detected with assay kit.Results After 4 h incubation,high glucose inhibited H9 c2 myocardial cell proliferation,promoted cell apoptosis,decreased the protein expression of c-Src and PI3 K,and increased the phosphorylation of ERK protein,but had no obvious effect on senescence,autophagy and total ERK protein of H9 c2 cells.Conclusion Hyperglycemia induces apoptosis and impaired proliferation of cardiac cells through dysfunction of c-Src/PI3 K/ERK pathway.

关 键 词：心肌细胞 H9C2 高糖 凋亡 c-Src PI3K ERK通路 

分 类 号：R363[医药卫生—病理学]