基础医学与临床 ›› 2019, Vol. 39 ›› Issue (7): 1025-1030.

• 研究论文 • 上一篇    下一篇

过表达PTEN抑制丙泊酚对过氧化氢诱导H9c2心肌细胞凋亡的保护作用

刘宇,何雨,李耀,万永灵   

  1. 四川省人民医院
  • 收稿日期:2018-06-07 修回日期:2018-10-30 出版日期:2019-07-05 发布日期:2019-07-02
  • 通讯作者: 万永灵 E-mail:wanyongling318@163.com
  • 基金资助:
    Neurexin-1β和Neuroligin-1在术后认知功能障碍中的作用

Over-expression of PTEN inhibits the protective effect of propofol against the apoptosis of H9c2 cardiacmyocytes induced by hydrogen peroxide

  • Received:2018-06-07 Revised:2018-10-30 Online:2019-07-05 Published:2019-07-02

摘要: 目的 探讨第10号染色体同源缺失性磷酸酶-张力蛋白(PTEN)对H2O2或丙泊酚诱导的H9C2心肌细胞凋亡的影响。方法 将H9C2心肌细胞分为对照组(正常培养细胞)、H2O2组(100 μmol/L H2O2孵育24 h)、丙泊酚5、10和30 μmol/L干预组,其中丙泊酚5、10和30 μmol/L干预组细胞分别经H2O2处理24h后加入不同浓度丙泊酚(5 μmol/L、10 μmol/L、30 μmol/L)预处理1 h。MTT法检测细胞的活力;流式细胞计量术检测细胞凋亡率;RT-qPCR检测PTEN mRNA;检测过表达PTEN对丙泊酚处理的H2O2诱导的心肌细胞活力、凋亡、乳酸脱氢酶(LDH)和活性氧(ROS)的影响。 结果 与对照组相比,5 μmol/L和10 μmol/L丙泊酚能提高H2O2诱导的心肌细胞活力、降低其凋亡率、抑制PTEN的表达量(P<0.05)。30 μmol/L丙泊酚显著抑制细胞活力、促进细胞凋亡和PTEN的表达量(P<0.05);过表达PTEN可抑制丙泊酚对H2O2诱导的H9C2细胞的保护作用(P<0.05),促进LDH和ROS的表达量(P<0.05)。结论 PTEN抑制丙泊酚对H2O2诱导的心肌细胞凋亡的保护作用。

关键词: H9C2心肌细胞, 丙泊酚, LDH, PTEN

Abstract: Objective To investigate the effect of phosphatase and tensin homolog deleted on chromosome 10(PTEN) on the apoptosis of H9C2 cardiomyocytes induced by H2O2. Methods H9C2 cardiomyocytes were divided into control group (normal cultured cells), H2O2 group (100 μmol/L H2O2 treatment for 24 h), propofol (5, 10, 30 μmol/L) group were treated with H2O2 for 24 h and then pretreated with propofol of different concentrations (5, 10, 30 μmol/L) for 1 h. The viability of cells was detected by MTT assay and the apoptosis rate was measured by flow cytometry. The expression of PTEN was detected by RT-qPCR; The viability, apoptosis, lactate dehydrogenase (LDH) , and reactive oxygen species (ROS) were analyzed of overexpression of PTEN. Results Compared with 0 μmol/L, 5 μmol/L and 10 μmol/L propofol significantly increased the activity of cardiomyocytes induced by H2O2, decreased the rate of apoptosis, and inhibited the expression of PTEN (P<0.05); 30 μmol/L propofol significantly inhibited cell viability and promoted apoptosis and the expression of PTEN (P<0.05); overexpression of PTEN could inhibit the protective effect of propofol against H2O2-induced H9C2 cells (P<0.05), and promote the expression of LDH and ROS (P<0.05). Conclusion PTEN inhibits the protective effect of propofol against H2O2-induced apoptosis of cardiomyocytes.

Key words: H9C2 cardiomyocytes, Propofol, LDH, PTEN