[1]王国权,庞素秋,邱飞,等.熊果酸对心肌缺血再灌注损伤的H9c2细胞的保护作用(英文)[J].华侨大学学报(自然科学版),2018,39(1):62-69.[doi:10.11830/ISSN.1000-5013.201706047]
　WANG Guoquan,PANG Suqiu,QIU Fei,et al.Protection of Ursolic Acid on Myocardial Ischemia/Reperfusion Injury in H9c2 Cells[J].Journal of Huaqiao University(Natural Science),2018,39(1):62-69.[doi:10.11830/ISSN.1000-5013.201706047]
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熊果酸对心肌缺血再灌注损伤的H9c2细胞的保护作用(英文)()
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《华侨大学学报（自然科学版）》[ISSN:1000-5013/CN:35-1079/N]

卷:
第39卷
期数:
2018年第1期
页码:
62-69
栏目:
出版日期:
2018-01-17

文章信息/Info

Title:
Protection of Ursolic Acid on Myocardial Ischemia/Reperfusion Injury in H9c2 Cells
文章编号:
1000-5013(2018)01-0062-08
作者:
王国权1; 2;  庞素秋3;  邱飞1; 2;  成文召1; 2;  杨会勇1; 2;  刁勇1; 2
1. 华侨大学 生物医学学院, 福建 泉州 362021;2. 华侨大学 医学院, 福建 泉州 362021;3. 中国人民解放军第180医院 临床药学科, 福建 泉州 362000
Author(s):
WANG Guoquan1; 2;  PANG Suqiu3;  QIU Fei1; 2;  CHENG Wenzhao1; 2;  YANG Huiyong1; 2;  DIAO Yong1; 2
1. School of Biomedical Sciences, Huaqiao University, Quanzhou 362021, China; 2. School of Medcine, Huaqiao University, Quanzhou 362021, China; 3. Department of Clinical Pharmacy, The 180th Hospital of People’s Liberation Army, Quanzhou 362000, China
关键词:
熊果酸;  心肌缺血/再灌注损伤;  细胞凋亡;  活性氧;  钙离子
Keywords:
ursolic acid;  myocardial ischemia/reperfusion injury;  apoptosis;  reactive oxygen species;  Ca2+
分类号:
U491.17
DOI:
10.11830/ISSN.1000-5013.201706047
文献标志码:
A
摘要:
为研究熊果酸(UA)对H9c2细胞心肌缺血/再灌注的影响,将细胞分为对照组、心肌缺血再灌注组(I/R)、熊果酸组(10,20,40 μmol·L-1)和尼莫地平阳性对照组(5 μmol·L-1).在细胞缺氧和复氧之前给药6 h后,经CCK-8检测细胞的增殖能力,采用流式细胞术检测钙离子(Ca2+)摩尔浓度、活性氧(reactive oxygen species,ROS)的产生及细胞凋亡情况.结果发现,UA对心肌缺血/再灌注细胞损伤的细胞具有明显的保护作用,其主要通过抑制细胞中细胞因子和趋化因子的释放,进而抑制I/R受损细胞的凋亡.蛋白质免疫印迹实验结果显示,与I/R组相比,UA能够显著诱导细胞中SLC8A2,RyR1,RyR2及Bcl-2的表达,抑制剪切型Caspase-3,Cyt-c,p-ERK1/2和p-p38蛋白的表达,且随着UA浓度升高趋势愈明显,表明UA对H9c2细胞的I/R损伤的保护作用具有浓度依赖性.UA促进细胞增殖和对心肌缺血/再灌注损伤的H9c2细胞保护作用可能与细胞中Ca2+摩尔浓度及ROS值降低有关,其主要机制可能通过ERK1/2和p-38信号通路介导.该研究能为UA保护H9c2细胞免受I/R损伤提供依据.
Abstract:
To investigate the effects of ursolic acid(UA)against myocardial ischemia-reperfusion in H9c2 cells, cells were divided into six groups: control group, myocardial ischemia reperfusion group, UA(10, 20, or 40 μmol·L-1)group, and nimodipine positive control group(5 μmol·L-1). The activity of cell proliferation was determined by CCK-8, and the flow cytometer analysis was employed to determine Ca2+ concentration, reactive oxygen species(ROS)production and cell apoptosis after 6 h when the drugs were given before the hypoxia reoxygenation of cells. The results showed that the UA treatment protected ischemia/reperfusion(I/R)injured cells from apoptosis remarkably via attenuating the release of cytokines and chemokines, Ca2+ overload and ROS generation. Furthermore, western blot showed that UA could significantly induced SLC8A2, RyR2 and RyR1 activity. Compared with the I/R group, the activity of Bcl-2 also increased significantly, and the activity of cleaved Caspase-3, Cyt-c, p-ERK 1/2 and p-p38 all decreased. These results suggest that UA has dose-dependent protective effects against myocardial I/R injury in H9c2 cells. Therefore, these findings provided evidence that UA could protect H9c2 cells from I/R injury, and the pro-proliferation and anti-apoptotic effects of UA might be mediated through decrease of ROS generation by Ca2+ content by activation of ERK 1/2 and p38 pathways.

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备注/Memo

备注/Memo:
收稿日期: 2017-06-24
通信作者: 庞素秋(1972-),女,副主任药师,博士,主要从事临床药学和天然药物的研究.E-mail:pangsuqiu@hqu.edu.cn
基金项目: 国家自然科学基金资助项目(81371669); 国家自然科学基金促进海峡两岸科技合作联合基金资助项目(U1405215)http://www.hdxb.hqu.edu.cn
更新日期/Last Update: 2018-01-20