| 引用本文: |
崔丽霞,孙丽萍,赵丕文,刘欣,石丹宁,陈梦.羟基红花黄色素A对氧化应激损伤血管内皮细胞的保护作用研究[J].湖南中医药大学学报,2019,39(4):475-479[点击复制] |
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| 羟基红花黄色素A对氧化应激损伤血管内皮细胞的保护作用研究 |
| 崔丽霞,孙丽萍,赵丕文,刘欣,石丹宁,陈梦 |
| (北京中医药大学, 北京 102488;北京中医药大学第三附属医院, 北京 100029) |
| 摘要: |
| 目的 探讨羟基红花黄色素A （hydroxysafflor yellow A，HSYA）对血管内皮细胞氧化应激损伤的保护作用及其可能机制。方法 体外培养人血管内皮细胞EC-304，用H2O2构建细胞氧化应激损伤模型，分别设置正常对照组、H2O2损伤模型组、HSYA药物组，其中各药物组用不同浓度的HSYA预培养细胞24 h后加入50 μmol/L的H2O2，继续培养12 h。用MTT法检测细胞的增殖活力，用试剂盒检测各组细胞内超氧化物歧化酶（SOD）、一氧化氮（NO）的含量，用Western Blot法检测各组细胞Bax、Bcl-2、Caspase-3、cleaved Caspase-3蛋白表达水平。结果 与H2O2模型组相比，HSYA能显著提高细胞存活率，且呈剂量依赖性，提高细胞内SOD的活性，提高细胞内NO的含量，降低Bax表达，提高Bcl-2表达，降低Caspase-3和cleaved Caspase-3的表达（P<0.01或P<0.05）。结论 HSYA对于H2O2诱导的血管内皮细胞氧化应激损伤具有保护作用，其可能的作用机制与抑制EC-304细胞凋亡相关。 |
| 关键词: 羟基红花黄色素A 血管内皮细胞 氧化应激损伤 细胞凋亡 |
| DOI：10.3969/j.issn.1674-070X.2019.04.009 |
| 投稿时间：2018-10-11 |
| 基金项目:北京中医药大学中央高校基本科研业务费专项资金资助（2017-JYB-JS-001）；国家自然科学基金（81673764） |
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| Protective Mechanism of Hydroxysafflor Yellow A on Vascular Endothelial Cells Injured by Oxidative Stress |
| CUI Lixia,SUN Liping,ZHAO Piwen,LIU Xin,SHI Danning,CHEN Meng |
| (Beijing University of Chinese Medcine, Beijing 102488, China;The Third Affiliated Hospital of Beijing Univesity of Chinese Medicine, Beijing 100029, China) |
| Abstract: |
| Objective To study the protective mechanism of hydroxysafflor yellow A (HSYA) on vascular endothelial cells injured by oxidative stress. Methods EC-304 human vascular endothelial cells were cultured in vitro. An oxidative stress injury model was established with H2O2. The cells were divided into several groups, namely control group, H2O2 injury model group, and HSYA groups. The cells in HSYA groups were pre-cultured with different concentrations of HSYA for 24 h, followed by addition of 50 μmol/L H2O2, and the cells were then cultured for another 12 h. Cell proliferation activity was determined by MTT assay, the content of superoxide dismutase (SOD) and nitric oxide (NO) was measured by kits, and the protein expression levels of Bax, Bcl-2, Caspase-3, and cleaved Caspase-3 were determined by Western Blot. Results Compared with the H2O2 model group, HSYA significantly increased the cell survival rate in a dose-dependent manner, and it significantly increased SOD activity, NO content, and Bcl-2 expression and significantly reduced the expression of Bax, Caspase-3, and cleaved Caspase-3 (P<0.01 or P<0.05). Conclusion HSYA has a protective effect on H2O2-induced oxidative stress injury of vascular endothelial cells, and the mechanism is possibly related to inhibition of the apoptosis of EC-304 cells. |
| Key words: hydroxysafflor yellow A vascular endothelial cell oxidative stress injury apoptosis |
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