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中国临床药理学与治疗学 ›› 2009, Vol. 14 ›› Issue (6): 613-616.

• 基础研究 • 上一篇    下一篇

甲胺鸢尾素对H2O2损伤大鼠心肌细胞线粒体膜电位的影响

郝言杰, 王元书, 牟艳玲, 解砚英, 张强, 周玲   

  1. 山东省医学科学院药物研究所药理室, 济南 250062, 山东
  • 收稿日期:2009-05-12 修回日期:2009-07-10 出版日期:2009-06-26 发布日期:2020-10-27
  • 通讯作者: 牟艳玲, 女, 博士, 助理研究员, 研究方向:心脑血管药理学。Tel:0531-82612443 E-mail:myling332@yahoo.com.cn
  • 作者简介:郝言杰,男,硕士研究生,研究方向:心血管药理学。Tel:15953127831 E-mail:haoyanjie@sina.com
  • 基金资助:
    国家自然科学基金资助项目(30701022);山东省自然科学基金项目(Y2007C156)

Effects of methylamine irisolidone on mitochondrial membrane potential in H2O2-induced rat cadiocyte injury

HAO Yan-jie, WANG Yuan-shu, MU Yan-ling, XIE Yan-ying, ZHANG Qiang, ZHOU Ling   

  1. Department of Pharmacology, Institute of Materia Medica, Shandong Academy of Medical Sciences, Jinan 250062, Shandong, China
  • Received:2009-05-12 Revised:2009-07-10 Online:2009-06-26 Published:2020-10-27

摘要: 目的: 研究新型化合物甲胺鸢尾素(methylamine irisolidone, MMI)预处理对H2O2损伤大鼠心肌细胞线粒体膜电位变化的影响。方法: 甲胺鸢尾素预处理心肌细胞12 h 后, 采用H2O2诱导细胞氧化应激损伤, 瑞氏-吉姆萨染色观察细胞形态,MTT 法检测细胞存活率, 流式细胞仪检测细胞线粒体膜电位变化。结果: 与正常对照组比较, 模型组心肌细胞存活率明显降低(P<0.01)。MMI0.1 μmol/L 组与模型组相比细胞存活率相近(P>0.05), 0.5、1、5、10 μmol/L 组显著增高(P<0.05, P<0.01)。与模型组比较, 10 μmol/L MMI减轻细胞形态变化, 1、5、10 μmol/L MMI 显著抑制线粒体膜电位下降(P<0.05, P<0.01)。结论: 甲胺鸢尾素可改善H2O2所致心肌细胞氧化应激损伤, 其机制与稳定细胞膜、抑制线粒体膜电位下降, 进而抑制心肌细胞凋亡有关。

关键词: 甲胺鸢尾素, 心肌细胞, 线粒体膜电位, 氧化应激, 细胞凋亡

Abstract: AIM: To investigate the protective effect of methylamine irisolidone(MMI)preconditioning on mitochondrial membrane potential in H2O2-induced rat cardiomyocytes injury. METHODS: With the pretreatment of methylamine irisolidone for 12 h in the model of H2O2-induced injury, the cell viability was determined by MTT assay, and the morphology change was examined with Wright's staining and Giemsa's staining, and the change of mitochondrial membrane potential was analyzed by flow cytometry. RESULTS: Compared with the normal group, the cell viability of model group was significantly decreased (P<0.01). Pretreated with methylamine irisolidone (0.5, 1, 5, 10 μmol/L)the cell viabilities were increased significantly (P<0.05, P<0.01), but MMI 0.1 μmol/L group had the similar cell viability compared with the model group (P>0.05).Moreover, pretreated with methylamine irisolidone (1, 5, 10 μmol/L)the mitochondrial membrane potential were increased (P<0.05, P<0.01), and 10 μmol/L group reduced the cell morphology injury. CONCLUSION: Methylamine irisolidone can improve the morphology injury of cadiocytes induced by H2O2 and increase the mitochondrial membrane potential, which can decrease the cadiocyte apoptosis.

Key words: methylamine irisolidone, cadiocyte, mitochondrial membrane potential, oxidative stress, apoptosis

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