人参皂甙Rg1对大鼠海马神经元缺糖氧/复糖氧后氧化损伤的保护作用

目的观察人参皂甙Rg1 对大鼠海马神经元缺糖氧/复糖氧后谷胱甘肽(GSH)和谷胱甘肽过氧化物酶(GPx)的影响。方法海马神经元培养8~10 d，随机分为正常对照组、模型组、人参皂甙Rg1 低、中、高剂量组(5 μmol/L, 20 μmol/L, 60 μmol/L)。建立大鼠海马神经元缺糖氧/复糖氧模型，复糖氧后6 h 以生物化学法观察各组海马神经元GSH含量和GPx活性的变化；复糖氧后24 h 以Hochest 染色法检测细胞凋亡，并检测各组海马神经元四甲基偶氮唑盐(MTT)代谢率。结果与模型组相比，人参皂甙Rg1中、高剂量组海马神经元GSH含量、GPx活性显著升高，凋亡显著减少，MTT代谢率显著提高(P<0.001)，人参皂甙Rg1 低剂量组变化不明显(P>0.05)。结论人参皂甙Rg1 可通过提高缺糖氧神经元GSH含量和GPx活性，发挥脑保护作用。

Neuroprotective Effect of Ginsenoside Rg1 on Oxidative Damage Induced by Oxygen-glucose Deprivation and Reperfusion in Cultured Hippocampal Cells

Objective To explore the effect of Ginsenoside Rgl on glutathion (GSH) level and glutathion peroxidase (GPx) activity after oxygen-glucose deprivation/reperfusion in cultured hippocampal cells. Methods The model of oxygen-glucose deprivation and reperfusion were established with the hippocampal neurons of rats. They were randomly divided into control group, model group and Ginsenoside Rgl treatment groups (5 μmol/L, 20 μmol/L, 60 μmol/L). The GSH level and GPx activity were measured 6 h after reperfusion. The apoptosis and the metabolic rate of methyl thiazolyl tetrazolium (MTT) were detected 24 h after reperfusion. Results Compared with model group, the GSH level, GPx activity, and metabolic rate of MTT improved (P<0.001), and the apoptosis decreased in the Ginsenoside Rgl groups (P<0.001) except with the dosage of 5 μmol/L (P>0.05). Conclusion Ginsenoside Rgl can protect the brain from ischemia by increasing the GSH level and GPx activity.