黄连碱对过氧化氢损伤的血管内皮细胞保护作用

Abstract
Figure/Table
References (20)
Related Citation (15)

Download: PDF (948 KB) HTML (1 KB)
Export: BibTeX | EndNote (RIS)

Abstract Objective To investigate the protective effect and mechanism of coptisine on vascular endothelial cells induced by hydrogen peroxide (H2O2). Methods Human umbilical vein endothelial cells (EA.hy926) cultured in vitro were divided into control group, model group and drug administration group. The control group was added with fresh medium, and the model group was stimulated by H2O2 for 4 h. The drug-treated group was pretreated with different concentrations of coptisine (2.5, 5, 10, 20, 40 μmol/L) for 4 h, and then stimulated with H2O2 for 4 h. Cell viability was detected by MTS assay, intracellular reactive oxygen species (ROS) was detected by ROS fluorescent probe - dihydroethidine (DHE) staining, apoptosis was detected by Annexin V-FITC/PI double staining, and Western blot was used to detect the changes of apoptosis-related proteins caspase-3, Bcl-2 and Bax. Results Compared with the control group, the cell viability and Bcl-2 protein levels of the model group were markedly decreased, whereas the ROS levels, apoptotic rate, caspase-3 and Bax protein levels were significantly increased (P < 0.01). However, compared with the model group, the cell viability and Bcl-2 protein levels of dosing group were increased gradually with the increasing concentration of coptisine, while the ROS levels, apoptotic rate, caspase-3 and Bax protein levels were decreased gradually with the increasing concentration of coptisine (P < 0.01). Conclusion Coptisine exerts its protective effect on vascular endothelial cells injured by H2O2 in a dose-dependent manner by inhibiting the decrease of survival rate, the increase of ROS, the increase of apoptotic rate, the up-regulation of caspase-3 and Bax protein expression and the down-regulation of Bcl-2 protein expression in EA.hy926 cells induced by H2O2.

Key words： Coptisine EA.hy926 cell Oxidative stress Apoptosis

	Service

	E-mail this article
	Add to my bookshelf
	Add to citation manager
	E-mail Alert
	RSS
	Articles by authors
	WEI Sheng LIU Jinchun GE Weihong

Cite this article:

WEI Sheng LIU Jinchun GE Weihong. Protective effect of coptisine on vascular endothelial cells injured by hydrogen peroxide[J]. 中国医药导报, 2019, 16(3): 4-7,21.

URL:

http://www.yiyaodaobao.com.cn/EN/ OR http://www.yiyaodaobao.com.cn/EN/Y2019/V16/I3/4

[1] Dahlöf B. Cardiovascular disease risk factors：epidemiology and risk assessment [J]. Am J Cardiol，2010，105（1）：3A-9A.
[2] Ganz P，Hsue PY. Endothelial dysfunction in coronary heart disease is more than a systemic process [J]. Eur Heart J，2013，34（27）：2025-2027.
[3] Kim H，Yun J，Kwon SM. Therapeutic Strategies for Oxidative Stress-Related Cardiovascular Diseases：Removal of Excess Reactive Oxygen Species in Adult Stem Cells [J]. Oxid Med Cell Longev，2016，2016（5）：2 483 163.
[4] Kelly FJ，Fussell JC. Role of oxidative stress in cardiovascular disease outcomes following exposure to ambient air pollution [J]. Free Radical Biol Med，2017，110：345-367.
[5] 张志辉，邓安珺，于金倩，等.黄连碱药理活性研究进展[J].中国中药杂志，2013，38（17）：2750-2754.
[6] Gong LL，Fang LH，Wang SB，et al. Coptisine exert cardioprotective effect through anti-oxidative and inhibition of RhoA/Rho kinase pathway on isoproterenol-induced myocardial infarction in rats [J]. Atherosclerosis，2012， 222（1）：50-58.
[7] Guo J，Wang SB，Yuan TY，et al. Coptisine protects rat heart against myocardial ischemia/reperfusion injury by suppressing myocardial apoptosis and inflammation [J]. Atherosclerosis，2013，231（2）：384-391.
[8] Libby P，Ridker PM，Hansson GK. Progress and challenges in translating the biology of atherosclerosis [J]. Nature，2011，473（7347）：317-325.
[9] Camaré C，Pucelle M，Nègre-Salvayre A，et al. Angiogenesis in the atherosclerotic plaque [J]. Redox Biol，2017，12：18-34.
[10] Förstermann U，Xia N，Li H. Roles of Vascular Oxidative Stress and Nitric Oxide in the Pathogenesis of Atherosclerosis [J]. Circ Res，2017，120（4）：713-735.
[11] Ogura S，Shimosawa T. Oxidative Stress and Organ Damages [J]. Curr Hypertens Rep，2014，16（8）：452.
[12] 杨洋，刘亭，王文华，等.参芎葡萄糖注射液对H2O2诱导的H9c2细胞氧化损伤的保护作用[J].中国实验方剂学杂志，2016，22（8）：153-158.
[13] Zhang N，Zhang Y，Zhao S，et al. Septin4 as a novel binding partner of PARP1 contributes to oxidative stress induced human umbilical vein endothelial cells injure [J]. Biochem Bioph Res Co，2018，496（2）：621-627.
[14] 张伟，梁智辉.Annexin V-FITC/PI双标记与Hoechst33342/PI双标记流式细胞术检测细胞凋亡的比较[J].细胞与分子免疫学杂志，2014，30（11）：1209-1212.
[15] Mignotte B，Vayssiere JL. Mitochondria and apoptosis [J]. Febs J，2010，252（1）：1-15.
[16] Liu XR，Cao L，Li T，et al. Propofol attenuates H2O2-induced oxidative stress and apoptosis via the mitochondria- and ER-medicated pathways in neonatal rat cardiomyocytes [J]. Apoptosis，2017，22（5）：1-8.
[17] Dubey M，Nagarkoti S，Awasthi D，et al. Nitric oxide-mediated apoptosis of neutrophils through caspase-8 and caspase-3-dependent mechanism [J]. Cell Death Dis，2016，7（9）：e2348.
[18] Ashkenazi A，Fairbrother WJ，Leverson JD，et al. From basic apoptosis discoveries to advanced selective Bcl-2 family inhibitors [J]. Nat Rev Drug Discov，2017，16（4）：273.
[19] Ola MS，Nawaz M，Ahsan H. Role of Bcl-2 family proteins and caspases in the regulation of apoptosis [J]. Mol Cell Biochem，2011，351（1/2）：41-58.
[20] Wang Q，Zhang L，Yuan X，et al. The Relationship between the Bcl-2/Bax Proteins and the Mitochondria-Mediated Apoptosis Pathway in the Differentiation of Adipose-Derived Stromal Cells into Neurons [J]. PLoS One，2016，11（10）：e0 163 327.