主 办:北 京 中 医 药 大 学
ISSN 1006-2157 CN 11-3574/R

北京中医药大学学报 ›› 2018, Vol. 41 ›› Issue (8): 636-641.doi: 10.3969/j.issn.1006-2157.2018.08.004

• 博士之光 • 上一篇    下一篇

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*

吴鸿1,2, 雷震2, 高水波2, 张玲霞3, 代丽萍3#   

  1. 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
  • 收稿日期:2018-03-05 出版日期:2018-08-30 发布日期:2018-08-30
  • 通讯作者: 代丽萍,女,博士,教授,研究方向:中药品质评价与质量标准研究,E-mail: zzdai@163.com
  • 作者简介:吴鸿,男,博士,副教授
  • 基金资助:
    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)

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

Wu Hong1,2, Lei Zhen2, Gao Shuibo2, Zhang Lingxia3, Dai Liping3#   

  1. 1 Laboratory of Cell Imaging, Henan University of Chinese Medicine, Henan 450002, China;
    2 Second School of Clinical Medicine, Henan University of Chinese Medicine, Henan 450002, China;
    3 Henan University of Chinese Medicine, Henan 450046, China
  • Received:2018-03-05 Online:2018-08-30 Published:2018-08-30
  • Supported by:
    National Natural Science Foundation of China (No. 81473453, No.81673800), the Science & Technology Innovation Talents in Universities of Henan Province (No. 14HASTIT028), the Henan Science and Technology Project (No. 142102310040)

摘要: 目的 研究羟基红花黄色素A(HSYA)对H2O2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H2O2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H2O2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H2O2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H2O2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。

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

Abstract: 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 H9c2 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 H9c2 cells and defend against oxidative damage in cardiomyocytes. The mechanism may be related to down-regulation of miR-1.

Key words: hydroxysafflor yellow A, reactive oxygen species, apoptosis, miR-1, oxidative damage, H9c2 rat cardiomyocytes

中图分类号: 

  • R285.5