中国临床药理学杂志2024，Vol.40Issue(19)：2826-2830,5.DOI:10.13699/j.cnki.1001-6821.2024.19.014
洛伐他汀通过调控Akt通路对缺氧/复氧心肌细胞损伤的保护作用
Protective effects of lovastatin on hypoxia/reoxygenation cardiomyocyte injury by regulating Akt pathway
摘要
Abstract
Objective To investigate the protective effect of lovastatin on cardiomyocyte injury induced by hypoxia/reoxygenation and the regulation of protein kinase B(Akt)signal pathway.Methods Rat cardiomyocytes H9c2 were cultured in vitro,and divided into control group,model group,inhibitor group,combined group and experimental-L,-M,-H groups.Control group was cultured with normal medium,and the other 6 groups were treated with hypoxia/reoxygenation.Experimental-L,-M,-H groups were supplemented with 1,2 and 5 μmol·L-1 lovastatin,respectively;inhibitor group was supplemented with 1 μmol·L-1 LY294002;combined group was supplemented with 5 μmol·L-1 lovastatin and 1 pmol·L-1 LY294002.The cell viability was determined by thiazole blue assay,the apoptosis rate was determined by flow cytometry,and the expression level of phosphorylated Akt(p-Akt)was determined by Western blot.Results The cell viabilities of experimental-H,inhibitor,combined,model and control groups were(64.38±7.10)％,(21.64±1.32)％,(51.89±2.25)％,(47.18±6.66)％and(100.00±7.69)％;the cell apoptosis rates were(13.67±1.42)％,(38.52±2.42)％,(21.12±2.27)％,(20.42±3.33)％and(4.93±0.40)％;the relative protein expression levels of p-Akt were 0.54±0.04,0.04±0.01,0.25±0.03,0.20±0.01 and 0.45±0.02,respectively.The differences of above indicators were statistically significant between the experimental-H group and the model group,as well as between the combined group and the experimental-H and inhibitor groups(all P＜0.05).Conclusion Lovastatin can protect against hypoxia/reoxygenation cardiomyocyte injury by activating the Akt signaling pathway.关键词
洛伐他汀/大鼠心肌细胞H9c2/缺氧/复氧/磷脂酰肌醇-3-激酶信号通路Key words
lovastatin/rat cardiomyocyte H9c2/hypoxia/reoxygenation/protein kinase B signaling pathway分类
医药卫生引用本文复制引用
韩小虎,腾丽峰,吴清柳,李儒正..洛伐他汀通过调控Akt通路对缺氧/复氧心肌细胞损伤的保护作用[J].中国临床药理学杂志,2024,40(19):2826-2830,5.基金项目
海南省自然科学基金资助项目(MS0828) （MS0828）
