白花丹醌对TBHP诱导的H9c2心肌细胞损伤的保护作用研究

Protective effect of plumbagin on H9c2 cardiomyocyte injury induced bytert-butyl hydroperoxide

目的:探讨白花丹醌(plumbagin, PLB)对叔丁基过氧化氢(TBHP)诱导的H9c2心肌细胞损伤的保护作用。方法:评估PLB对TBHP(75μmol·L^(-1))诱导的活性氧(ROS)介导的H9c2心肌细胞的氧化应激和细胞凋亡的保护作用。结果:用5,10和20μmol·L^(-1) PLB预处理后,可显著恢复TBHP诱导的H9c2细胞中的细胞活力,显著降低肌酸激酶(CK)和乳酸脱氢酶(LDH)活性。TBHP导致心肌细胞凋亡增加,而PLB预处理以剂量依赖性方式抑制TBHP诱导的细胞凋亡。此外,经PLB处理后,微管相关蛋白1a/1B轻链3B(LC3)-Ⅱ/LC3-Ⅰ的表达水平升高,提示PLB能够诱导心肌细胞自噬。结论:PLB对TBHP诱导的心肌细胞损伤具有保护作用,该作用可能与PLB抑制ROS介导的氧化应激、凋亡和自噬作用有关。

OBJECTIVE To explore the protective effect of plumbagin(PLB) on H9 c2 cardiomyocyte damage induced by tert-butyl hydroperoxide(TBHP).METHODS PLB was utilized for evaluating its cytoprotective property in H9 c2 cardiomyocytes against tertiary butyl hydrogen peroxide(TBHP, 75 μmol·L^(-1)) induced reactive oxygen species(ROS)-mediated oxidative stress and apoptosis.RESULTS A pretreatment of PLB(5/10/20 μmol·L^(-1)) significantly restored cellular viabilities in TBHP-induced H9 c2 cell. Also PLB treatment significantly lowered the activities of creatine kinase(CK) and lactate dehydrogenase(LDH). TBHP accelerated cardiomyocyte apoptosis while PLB dosing protected cells from TBHP-induced apoptosis in a dose-dependent manner. And the expression level of microtubule-associated proteins 1 a/1 B light chain 3 B(LC3)-Ⅱ/LC3-Ⅰ was elevated after a treatment of PLB.CONCLUSION The protective effect of PLB on TBHP-induced cardiomyocyte damage may be mediated through an inhibition of ROS-mediated oxidative stress, apoptosis and autophagy by PLB.