Neuroprotective effects of ginsenoside Rg1 against oxygen-glucose deprivation in cultured hippocampal neurons

被引:25
作者
He, Qing [1 ]
Sun, Jianguo [2 ]
Wang, Qin [2 ]
Wang, Wei [2 ]
He, Bin [3 ]
机构
[1] First Hosp Xuzhou, Dept Neurol, Xuzhou, Jiangsu, Peoples R China
[2] Nanjing Med Univ, Affiliated Hosp 1, Dept Neurol, Nanjing 210029, Jiangsu, Peoples R China
[3] Nanjing Med Univ, Affiliated Hosp 1, Emergency Ctr, Nanjing 210029, Jiangsu, Peoples R China
基金
中国国家自然科学基金;
关键词
calcium overload; cerebral ischemia; ginsenoside Rg1; hippocampal neurons; nitric oxide synthase; FOCAL CEREBRAL-ISCHEMIA; NITRIC-OXIDE; GLUTAMATE; CELLS; PHARMACOLOGY; ACTIVATION; APOPTOSIS; PATHWAY; SIGNALS; INFLUX;
D O I
10.1016/j.jcma.2014.01.001
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background: Ginsenoside Rg1 (Rg1) is believed to be one of the main active principles in ginseng, a traditional Chinese medicine extensively used to enhance stamina and deal with fatigue as well as physical stress. It has been reported that Rg1 performs multiple biological activities, including neuroprotective activity. In this study, we investigated the efficacy of ginsenoside Rg1 on ischemia-reperfusion injury in cultured hippocampal cells and also probed its possible mechanisms. Methods: To establish a model of oxygen-glucose deprivation (OGD) and reperfusion, cultured hippocampal neurons were exposed to OGD for 2.5 hours, followed by a 24-hour reoxygenation. Cultured hippocampal neurons were randomly divided into control group, model group (vehicle), and ginsenoside Rg1 treatment groups (5 mu M, 20 mu M, 60 mu M). At 24 hours post-OGD, the intracellular free calcium concentration was detected using Furo-3/AM-loaded hippocampal neurons deprived of oxygen and glucose. Neuronal nitric oxide synthase (nNOS) activity was measured by chemical colorimetry. Cell apoptosis was evaluated by Hoechst staining, and the neuron Viability was determined by 344,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Results: Excitotoxic neuronal injury of OGD was demonstrated by the increase of intracellular free calcium concentrations and elevated nNOS activity in the model group compared with the control group. The intracellular free calcium concentrations and the nNOS activity in the groups receiving intermediate and high dose of ginsenoside Rg1 were significantly lower than those of the control group (p < 0.05). In addition, intermediate and high dose of ginsenoside Rg1 administration could also attenuate the cell viability loss (p < 0.05) and cell apoptosis induced by OGD. Conclusion: Ginsenoside Rg1 has neuroprotective effect on ischemia reperfusion injury in cultured hippocampal cells mediated by blocking calcium over-influx into neuronal cells and decreasing the nNOS activity after OGD exposure. We infer that ginsenoside Rg1 may serve as a potential therapeutic agent for cerebral ischemia injury. Copyright (C) 2014 Elsevier Taiwan LLC and the Chinese Medical Association. All rights reserved.
引用
收藏
页码:142 / 149
页数:8
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