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中国临床药理学与治疗学 ›› 2006, Vol. 11 ›› Issue (7): 806-809.

• 研究原著 • 上一篇    下一篇

开放线粒体KATP通道对心肌细胞氧化应激损伤的保护作用

曾源, 龙超良1, 李艳芳2, 汪海1   

  1. 1解放军306 医院干部病房, 北京 100101;
    2军事医学科学院毒物药物研究所, 北京 100850;
    sup>3北京安贞医院十二病房, 北京 100720
  • 收稿日期:2006-05-20 修回日期:2006-06-26 出版日期:2006-07-26 发布日期:2020-10-30
  • 通讯作者: 汪海, 男, 医学博士, 研究员, 博士生导师, 从事心血管药理学和新药研究工作。Tel:010-66932651 E-mail:wh@nic.bmi.ac.cn
  • 作者简介:曾源, 女, 硕士研究生, 主治医师, 研究方向:老年心血管。Tel:010-66356307 E-mail:zyuan306@yahoo.com.cn

Protective effects of mitoKATP opener on cardiac myocytes damages induced

ZENG Yuan, LONG Chao-liang1, LI Yan-fang2, WANG Hai1   

  1. 1Department of Geratology , 306 Hospital of PLA, Beijing 100101 , China;
    2Institute of Pharmacology and Toxicology,Academy of Military Medical Sciences, Beijing 100850 , China;
    3Department of Cardiology , Anzhen Hospital , Beijing 100720 , China
  • Received:2006-05-20 Revised:2006-06-26 Online:2006-07-26 Published:2020-10-30

摘要: 目的 观察ATP 敏感性钾通道(KATP ) 开放剂二氮嗪对心肌细胞氧化应激损伤的保护作用, 并探讨其作用机制。方法 采用过氧化氢(500 μmol·L-1 )诱导法制备大鼠培养心肌细胞氧化应激损伤模型,通过检测培养液中乳酸脱氢酶以及用流式细胞仪结合罗丹明-123 和碘化丙啶双标记法检测线粒体膜电位和细胞存活状态, 观察二氮嗪(100 μmol·L-1 ) 对氧化应激损伤的保护作用。结果 二氮嗪预处理后,细胞培养液中乳酸脱氢酶活性较过氧化氢处理组显著降低(P<0.01) , 细胞存活率升高, 并可减少氧化应激造成的线粒体膜电位的丢失, 其作用可被线粒体KATP通道阻断剂5-羟基癸酸酯所拮抗。结论 二氮嗪对过氧化氢造成的培养心肌细胞氧化应激损伤具有保护作用, 其可能通过激活线粒体KATP 通道介导。

关键词: 二氮嗪, 线粒体ATP 敏感性钾通道, 心肌细胞, 氧化应激损伤

Abstract: AIM: To investigate the protective effects of Diazoxide, a selective mitoKATP opener, on the cardiac myocytes damages induced by oxidative stress and to discuss its mechanism.METHODS: Oxidative damage cell model was induced by hydrogen peroxide (H2O2 500 μmol·L-1).Lactate dehydrogenase (LDH) activities in the medium and mitochondrial membrane potential assessed in flow cytometry by dual labelling with rhodamine-123 (Rh-123) and propidium were measured in the diazoxide(100 μmol·L-1 ) pretreated and un-pretreated groups.RESULTS: The level of LDH and the percentage of injured cells in H2O2 exposure group after 2 h injury were significantly higher than those in the control group(P<0.01).On the contrary, after exposure to H2O2 ,the Rh-123 fluorescence intensity was significantly decreased.Compared with simple injury group, pre-treatmentwith diazoxide (100 μmol·L-1 ) could obviously attenuateH2O2 induced cytotoxicity, which could be abrogated by the mitoKATP channel blocker 5-hydroxydecanoate(500 μmol·L-1).CONCLUSION: Diazoxide exerts significant protective effects against the damages induced by H2O2 in the cultured neonatal rat cardiomyocytes,which may be mediated by activation of mitoKATP channels.

Key words: diazoxide, mitoKATP channels, myocardial cell, oxidative stress

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