文章摘要
王海云,王俏,王代明,朱健,朱虹.丹参多酚酸盐对过氧化氢诱导的血管内皮细胞损伤的影响及其机制[J].中国临床保健杂志,2020,23(6):831-834.
丹参多酚酸盐对过氧化氢诱导的血管内皮细胞损伤的影响及其机制
Effects of salvianolate on the vascular endothelial cell injury induced by H2O2 and its mechanisms
投稿时间:2020-04-27  
DOI:10.3969/J.issn.1672-6790.2020.06.027
中文关键词: 急性肺损伤  内皮细胞  氧化性应激
英文关键词: Acute lung injury  Endothelial cells  Oxidative stress〖FL
基金项目:
作者单位E-mail
王海云 上海交通大学医学院附属第九人民医院急诊科,上海 200011 zhuhong1096@126.com 
王俏 上海交通大学医学院附属第九人民医院急诊科,上海 200011 zhuhong1096@126.com 
王代明 上海市公惠医院内科 zhuhong1096@126.com 
朱健 上海交通大学医学院附属第九人民医院急诊科,上海 200011 zhuhong1096@126.com 
朱虹 上海交通大学医学院附属第九人民医院·临床医学院 zhuhong1096@126.com 
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中文摘要:
      目的 探讨丹参多酚酸盐对过氧化氢(H2O2)诱导的血管内皮细胞损伤的影响及其机制。方法 人脐静脉内皮细胞(HUVEC)分成三组:对照组,H2O2组(H2O2处理)和丹参多酚酸盐组(丹参多酚酸盐+H2O2处理)。通过CCK8法检测各组细胞增殖情况;各组细胞处理72 h后,通过紫外分光光度法检测各组细胞的超氧化物歧化酶(SOD)和丙二醛(MDA)的含量,定量PCR检测各组细胞炎性因子白细胞介素-6(IL-6)、白细胞介素-1β(IL-1β)、血清肿瘤坏死因子-α(TNF-α)和核因子E2相关因子(Nrf2)的表达水平。结果 与H2O2组相比,丹参多酚酸盐能显著逆转H2O2诱导的HUVEC细胞增殖抑制,降低细胞内 MDA的水平,降低炎性因子IL-6、IL-1β、TNF-α的表达,增加细胞内SOD的水平和Nrf2的表达,差异均有统计学意义(P值均<0.05)。结论 丹参多酚酸盐对H2O2诱导的血管内皮细胞的氧化应激损伤和炎性损伤具有保护作用,其机制可能与上调Nrf2的表达有关。
英文摘要:
      Objective To investigate the effects of salvianolate on the vascular endothelial cell injury induced by H2O2 and its mechanisms.Methods Human umbilical vein endothelial cells (HUVEC) were divided into three groups,control group,H2O2 treated group and salvianolate and H2O2 treated group.Cell proliferation was detected by a CCK assay.After 72 hours,the levels of SOD and MDA in those groups were detected.The expressions of IL-6,IL-1β,TNF-α and Nrf2 were detected by quantitative real-time PCR.Results Compared with H2O2 treated group,salvianolate reversed the inhibitory effect of H2O2 on HUVEC cells.Salvianolate suppressed the level of MDA and expression of IL-6,IL-1β and TNF-α in HUVEC cells induced by H2O2.Salvianolate increased the level of SOD and Nrf2 in HUVEC cells induced by H2O2.These indexes are statistically significant(P<0.05).Conclusion Salvianolate possesses a protective effect against H2O2-induced oxidative damage and inflammatory injury of HUVEC through regulation of Nrf2.
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