仙茅苷对H2O2氧化损伤心肌细胞的保护作用

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。

Protective effect of curculigoside on cardiomyocyte oxidative injury induced by H2O2

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.