羟基红花黄色素A通过抑制微小RNA-1表达对H9c2心肌细胞氧化损伤的保护作用  

Protective effects of hydroxysafflor yellow A on oxidative damage in H9c2 cells through inhibiting microRNA-1

作　　者：吴鸿[1,2] 雷震 高水波 张玲霞 代丽萍[3] Wu Hong;Lei Zben;Gao Shuibo;Zhang Lingxia;Dai Liping(Laboratory of Cell Imaging,Henan University of Chinese Medicine,Henan 450002,China;Second Sehool of Clinical Medicine,Henan University of Chinese Medicine,Henan 450002,China;Henan University of Chinese Medicine,Henan 450046,China)

机构地区：[1]河南中医药大学细胞成像实验室,河南450002 [2]河南中医药大学第二临床医学院 [3]河南中医药大学

出　　处：《北京中医药大学学报》2018年第8期636-641,共6页Journal of Beijing University of Traditional Chinese Medicine

基　　金：国家自然科学基金资助项目(No.81473453;No.81673800);河南省高校科技创新人才支持计划(No.14HASTIT028);河南省科技攻关项目(No.142102310040)~~

摘　　要：目的研究羟基红花黄色素A(HSYA)对H_2O_2诱导的心肌细胞氧化损伤的保护作用,进一步观察该作用与微小RNA-1(miR-1)之间的关系。方法以细胞存活率为指标筛选HSYA的最适浓度。将细胞分为空白组、模型组、羟基红花黄色素A干预组,荧光显微镜检测活性氧(ROS)水平、流式细胞仪检测凋亡率、实时荧光PCR法检测miR-1表达水平,研究HSYA对H_2O_2氧化损伤的心肌细胞的保护作用。在此基础上,研究miR-1模拟物转染心肌细胞情况下H_2O_2诱导损伤后miR-1与ROS水平,及HSYA对细胞损伤的保护作用。结果与空白组比较,模型组ROS水平升高,凋亡率增加,miR-1表达上调,差异有统计学意义。与模型组比较,羟基红花黄色素A干预组ROS水平降低,凋亡率降低,miR-1表达下调,差异有统计学意义。H9c2细胞被转染miR-1模拟物后,miR-1水平升高,ROS生成增多,与H_2O_2诱导的miR-1水平升高和ROS生成增多呈叠加效应,而HSYA对其叠加升高的miR-1及ROS水平有下调作用。结论 HSYA能够降低H_2O_2诱导的H9c2细胞ROS生成和细胞凋亡率,对心肌细胞氧化损伤起保护作用,其机制可能与下调miR-1表达水平有关。Objective To investigate the protective effect of hydroxysafflor yellow A（ HSYA） on oxidative damage in cardiomyocytes,and to further observe the relationship between this effect and microRNA-1（ miR-1）. Methods The optimal concentration of HSYA was firstly screened by cell viability. The cells were divided into blank group,model group and HSYA group. The level of reactive oxygen species（ ROS） was detected by using fluorescence microscope; the rate of apoptosis was measured with flow cytometry and the expression of miR-1 was determined by real-time q-PCR,on which the protective effect of HSYA on myocardial cells injured by H2O2 was clarified. Furthermore,the level of miR-1 and ROS in miR-1 mimic-transfecting myocardial cells injured by H2O2 was explored,as well as the effect of HSYA on the injuries. Results Compared with the blank group,the level of ROS,apoptosis rate,and miR-1 expression all increased in model group,and the differences were statistically significant. Compared with model group,the level of ROS,apoptosis rate and miR-1 expression all decreased in HSYA group,and the differences were also statistically significant. After the transfection of H9 c2 cells with miR-1 mimics,the level of miR-1 and ROS increased,which was superimposed on the level of miR-1 and ROS induced by H2O2,while HSYA downregulated the level of miR-1 and ROS. Conclusion HSYA can reduce the level of ROS generation and apoptosis induced by H2O2 in H9 c2 cells and defend against oxidative damage in cardiomyocytes. The mechanism may be related to down-regulation of miR-1.

关 键 词：羟基红花黄色素A 活性氧 细胞凋亡 微小RNA-1 氧化损伤 H9c2大鼠心肌细胞 

分 类 号：R285.5[医药卫生—中药学]