芝麻素含药血清对血管紧张素Ⅱ诱导大鼠心肌细胞凋亡的影响

Effect of Serum Containing Sesamin on Angiotensin Ⅱ-Induced Apoptosis in Rat Cardiomyocytes

目的:观察芝麻素含药血清对血管紧张素Ⅱ(AngⅡ)诱导大鼠心肌细胞凋亡的影响,并探讨其可能机制。方法:培养H9C2大鼠心肌细胞,与芝麻素含药血清或空白血清预孵12 h后,加入AngⅡ孵育24 h。MTT法检测心肌细胞活力,流式细胞术检测细胞凋亡率,Western blot法检测BCL-2、BAX、Caspase-3、SOD和p47phox蛋白表达水平,比色法测定细胞总抗氧化能力、细胞内活性氧(ROS)水平和丙二醛(MDA)含量。结果:芝麻素含药血清预孵可显著改善AngⅡ诱导的心肌细胞凋亡和活力损伤(P<0.05或P<0.01),下调BAX、Caspase-3及p47phox蛋白表达,上调BCL-2、SOD蛋白表达水平(P<0.05或P<0.01)。此外,芝麻素含药血清可显著提高心肌细胞总抗氧化能力降低细胞内ROS和培养上清MDA含量(P<0.05或P<0.01)。空白血清对上述指标均无显著影响。结论:芝麻素可显著抑制AngⅡ诱导的心肌细胞凋亡和活力损伤,其机制与改善氧化应激状态、调节BCL-2/BAX蛋白表达水平,进而下调Caspase-3蛋白表达有关。

Objective： To investigate the effect of serum containing sesamin on angiotension Ⅱ（ AngⅡ）-induced apoptosis in rat cardiomyocytes and the possible mechanisms. Methods： H9c2 rat cardiomyocytes were preincubated with serum containing sesamin or blank serum for 12 h,followed by incubation with AngⅡ for 24 h. Cell viability was assessed by MTT assay and cell apoptosis was evaluated by flow cytometric analysis. Protein expression of BCL-2,BAX,Caspase-3,p47 phox and superoxide dismutase（ SOD） was determined by Western blot analysis. Levels of intracellular reactive oxygen species（ ROS）,total antioxidant capacity（ T-AOC） and malondialdehyde（ MDA） were measured colorimetrically. Results： Preincubation with serum containing sesamin significantly improved cell viability and suppressed cell apoptosis in H9c2 rat cardiomyocytes exposed to AngⅡ（ P 0. 05 or P 0. 01）,with the expression of BAX,Caspase-3 and p47 phox protein down-regulated and BCL-2 and SOD protein up-regulated markedly（ P 0. 05 or P 0. 01）. The levels of T-AOC were effectively increased in serum containing sesamin groups,while the levels of intracellular ROS and MDA contents were decreased significantly（ P 0. 05 or P 0. 01）. Control serum had no influence on the above mentioned measurements. Conclusion： Sesamin is capable of suppressing AngⅡ-induced apoptosis in H9c2 rat cardiomyocytes,which might be derived,at least partly,from amelioration of oxidative stress,regulation of BAX / BCL-2 protein expression and suppression of Caspase-3 protein expression.