《中国康复理论与实践》 ›› 2012, Vol. 18 ›› Issue (12): 1112-1115.

• 论文 • 上一篇    下一篇

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

何斌,吴鸿浩,吕金如,孙昊,吴昊,蒋雷,王淦楠,胡德亮,张劲松,陈彦   

  1. 南京医科大学第一附属医院急诊科,江苏南京市210029。
  • 收稿日期:2012-07-31 修回日期:1900-01-01 出版日期:2012-12-25 发布日期:2012-12-25
  • 通讯作者: 陈彦

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

HE Bin, WU Hong-hao, LÜ Jin-ru, et al.   

  1. Department of Emergency, the First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, Jiangsu, China
  • Received:2012-07-31 Revised:1900-01-01 Published:2012-12-25 Online:2012-12-25

摘要: 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。

关键词: 脑缺血, 人参皂甙Rg1, 谷胱甘肽, 细胞凋亡, 海马

Abstract: 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.

Key words: cerebral ischemia, Ginsenoside Rg1, glutathion, apoptosis, hippocampus