仙茅苷对H_2O_2氧化损伤心肌细胞的保护作用

Protective effect of curculigoside on cardiomyocyte oxidative injury induced by H_2O_2

目的探讨仙茅苷对H2O2氧化损伤心肌细胞的保护作用及机制。方法体外培养大鼠原代心肌细胞,将其分为空白对照组、DMSO溶剂对照组(0.1%)、H2O2氧化损伤组(200μmol/L)、槲皮素干预组(槲皮素30μmol/L+H2O2200μmol/L)、低浓度仙茅苷干预组(仙茅苷0.5μmol/L+H2O2200μmol/L)、中浓度仙茅苷干预组(仙茅苷5μmol/L+H2O2μmol/L)、高浓度仙茅苷干预组(仙茅苷50μmol/L+H2O2200μmol/L)。用H2O2氧化损伤经槲皮素及不同浓度仙茅苷预培养24 h的心肌细胞,18 h后测定细胞培养液中乳酸脱氢酶(LDH)释放量、心肌细胞内丙二醛(MDA)和谷胱甘肽过氧化物酶(GSH-px)含量,并测定心肌细胞的凋亡率和生长抑制率。结果 H2O2氧化损伤后LDH、MDA含量明显升高,GSH-px活性明显下降,细胞抑制率和凋亡率均增加(P<0.01);而经槲皮素、不同浓度的仙茅苷预处理组的心肌细胞,LDH、M DA含量明显下降,GSH-px活性明显升高,细胞生长抑制率和凋亡率均降低(P<0.01);且仙茅苷对心肌细胞氧化损伤的保护作用呈浓度依赖性。结论仙茅苷预处理心肌细胞可保护H2O2所诱导的氧化损伤,其作用可能与抑制脂质过氧化、增加抗氧化酶活性、减少心肌细胞凋亡有关。

Objective To investigate the protective effect of curculigoside on oxidative injury of cardiomyocytes and its mechanism. Methods Primary cardiomyocytes were cultured in vitro,and divided into： control group,solvent group（DMSO,0. 1%）,oxidative injury group（H2O2200 μmol / L）,quercetin group（30 μmol / L with DMSO 0. 1%）,and curculigoside groups（ 0. 5,5,50 μmol / L）. After precultured of quercetin and various concentrations of curculigoside for 24 h,myocardial cells were incubated with 200 μmol / L H2O2 for 18 hours,the lactate dehydrogenase（ LDH） in culture medium,malondialdehyde（ M DA） and glutathione peroxidase（ GSH-px） in myocardial cells,cell apoptosis rate and growth inhibition rate were determined. Results Compared with control group,the LDH and M DA contents of oxidative injury group was significantly increased,GSH-px activity decreased,the cell apoptosis rate and growth inhibition rate were increased（ P〈0. 01）. Compared with oxidative injury group,LDH release and M DA content in quercetin and curculigoside groups were decreased,GSH-px activity increased,cell apoptosis rate and growth inhibition rate were decreased（ P〈0. 01）.Curculigoside presented protective effect on oxidative injury in a concentration-dependent manner.Conclusion Curculigoside can protect cardiomyocytes from oxidative injury induced by H2O2,which may be associated with its effects of inhibiting lipid peroxidation,increasing GSH-px activation and reducing cell apoptosis in myocardial cells.