摘要
目的:探究丹参酮ⅡA对大鼠心肌细胞H9C2氧化损伤的保护作用。方法:建立H2O2诱导大鼠心肌细胞H9C2氧化损伤模型。将体外培养的H9C2细胞随机分为空白对照组、DMSO溶剂对照组、H2O2模型组、丹参酮ⅡA高、中、低剂量组。用MTT法测定心肌细胞存活率,并检测培养液上清中乳酸脱氢酶(LDH)、超氧化物歧化酶(SOD)以及丙二醛(MDA)的水平。结果:与空白对照组相比,H2O2模型组细胞存活率显著降低,LDH、MDA水平升高,SOD水平降低;与H2O2模型组相比,丹参酮ⅡA高剂量组心肌细胞存活率显著增高,LDH和MDA水平降低,SOD水平升高(P<0.01)。结论:丹参酮ⅡA能够减轻心肌细胞氧化损伤。
Objective： To investigate the protective effects of tanshinone ⅡA on oxidative damage induced by hydrogen peroxide（ H2O2 ） in myocardial cells. Methods： Myocardial injury models in H9C2 cells induced by H2O2 were established. H9C2 cells cultured in vitro were randomly divided into six groups： normal group, DMSO solvent control group, H2O2 model group, tanshinone II A high, medium and low dose groups. The survival rate of myocardial cells was determined by MTT method. The levels of lactate dehydrogenase （LDH）, superoxide dismutase （SOD） and malondialdehyde （MI）A） were detected in the supernatant of the medium. Results： Compared with normal group, the survival rate of H9C2 myocardial cells in the H2O2 model group was significantly decreased. Furthermore, the levels of LDH and MDA were increased, while the level of SOD was decreased remarkably. Compared with H2O2 model group, the survival rate of H9C2 myocardial cells treated with high dose of tanshinone 11 A was increased. In addition, the levels of LDH and MDA were decreased, while the level of SOD was increased significantly （P 〈 0. 01 ）. Conclusion： Tanshinone ⅡA can protect myocardial cells from oxidative damage. [
出处
《国际心血管病杂志》
2015年第4期261-263,268,共4页
International Journal of Cardiovascular Disease
基金
长治医学院科技创新项目(CX2014-01)
山西省科学技术发展计划(20130321029-01)
