论文部分内容阅读
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(5μmol/L,20μmol/L,60μmol/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。
Objective To observe the effects of ginsenoside Rg1 on glutathione (GSH) and glutathione peroxidase (GPx) in rat hippocampal neurons after glucose deprivation / hyperglycemia. Methods Hippocampal neurons cultured for 8-10 days were randomly divided into normal control group, model group and low, medium and high doses of ginsenoside Rg1 (5μmol / L, 20μmol / L, 60μmol / L). The model of hypoglycemia / hyperglycemia was established in rat hippocampal neurons. The levels of GSH and GPx in hippocampal neurons were determined by biochemical method 6 h after ICH. Hochest staining was performed 24 h after ICH Apoptosis was detected and the MTT metabolic rate of hippocampal neurons in each group was measured. Results Compared with the model group, GSH and GPx activities of hippocampal neurons in Gg group were significantly increased (P <0.001), and the apoptosis rate was significantly decreased (P <0.001). The changes of Ginsenoside Rg1 low dose group Not obvious (P> 0.05). Conclusion Ginsenoside Rg1 can play a neuroprotective role by increasing GSH content and GPx activity in glucose-deprived oxygen neurons.