摘要
目的探讨消退素D1(RvD1)对H2O2诱导状态下H9C2心肌细胞血红素氧合酶-1(HO-1)的调节作用及相关的分子机制。方法将大鼠心肌H9C2细胞分为对照组、消退素D1+H2O2组(Resolvin D1+H2O2组)和H2O2组3组,在200μM的H2O2干预6小时后使用RT-PCR法和western blot法对各组H9C2心肌细胞HO-1mRNA和蛋白的表达水平进行检测;并使用western blot法对H9C2心肌细胞p38 MAPK磷酸化水平(Phospho-p38 MAPK/total p38MAPK比值)进行测量。结果与对照组比较,在H2O2干预6小时后H9C2心肌细胞HO-1mRNA和蛋白的表达水平明显降低,而p38 MAPK磷酸化水平均明显升高,差异均有统计学意义(均P<0.05);但H2O2组较Resolvin D1+H2O2组HO-1mRNA和蛋白表达的降低以及p38 MAPK磷酸化水平的增加更加显著,差异均有统计学意义(均P<0.05)。结论本研究结果表明,在过氧化氢诱导的H9C2心肌细胞氧化应激和损伤过程中消退素D1可能是通过抑制P38 MAPK的活化上调了HO-1的表达,对心肌细胞有保护作用。
Objective To investigate the role of resolvin D1（RevD1）on regulation of HO-1 expression in H2O2-induced injury and its potential mechanism in rat H9C2 cardiomyocytes.Methods H9C2 cardiomyocytes were divided into control group,RevD1＋H2O2 group and H2O2 group.After 6 hours H2O2 stimulation,RT-PCR was performed to analyze the mRNA expression of HO-1.Then,western blot was included to observe the protein expression of HO-1and the ratio of phospho-p38 MAPK/total p38 MAPK.Results After 6 hours H2O2 stimulation,the mRNA and protein expression of HO-1was sharply reduced,and the phosphorylation level of p38 MAPK was significantly promoted.Furthermore,H2O2-induced the reduction of HO-1 and the enhanced level of phospho-p38 MAPK were both improved by resovin D1 in rat H9C2 cardiomyocytes.Conclusion Resovin D1 increased the expression of HO-1 probably through inactivation of p38 MAPK in H9C2 cardiomyocytes in H2O2 stimulation condition.
出处
《西部医学》
2015年第3期331-334,共4页
Medical Journal of West China
基金
河北省卫生厅重点科技研究课题(20130359)
