Protective effect of ginsenoside Rb_1 on ischemic brain injury in rat

Protective effect of ginsenoside Rb_1 on ischemic brain injury in rat
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发表时间:
2003
期刊:
Journal of Apoplexy and Nervous Diseases
影响因子:
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通讯作者:
Jiang Zheng-li
Jiang Zheng-li
中科院分区:
其他
文献类型:
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作者:
Jiang Zheng-li

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目的采用离体大鼠海马脑片,通过电生理技术研究抗凋亡基因Rb 1对缺血性脑损伤的保护作用及其机制。方法(1)观察模拟脑缺血过程中及给予α-Rb-1后顺向群峰电位(OPS)的变化。(2)观察谷氨酸兴奋性毒性后OPS的变化及Rb 1的拮抗作用。结果(1)人参皂甙作用后OPS的变化:对照组在模拟缺血时,所有脑片均出现缺氧损伤电位(HIP),复氧后OPS略有恢复;人参皂甙Rb 1(600μmol/L)可减少HIP的出现,复氧后OPS的恢复率和幅度均显著高于对照组。(2)抗谷氨酸兴奋性毒性作用:对照组,1.5mmol/L谷氨酸使OPS幅值降低,暴露结束后OPS恢复率和幅值均较低,而600μmol/L抗谷氨酸兴奋性毒性作用后,OPS恢复率和幅值均较对照组显著升高。结论人参皂苷Rb 1对缺血性脑损伤具有保护作用。其作用机制与黄芪皂苷拮抗谷氨酸兴奋性毒性有关。
Objective Using rat hippocampal slices,the protective effect of ginsenoside Rb 1 on ischemic brain injury and the mechanism were investigated in vitro by means of electrophysiological technique. Methods (1)The changes of orthodromic population spike(OPS) during simulated ischemia and after administration of ginsenoside Rb 1 were observed. (2)The changes of OPS after exposure to Glutamate and the effect of ginsenoside Rb 1 aganist the Glutamate excitory toxicity were observed. Results (1)The changes of OPS after administration of ginsenosides:in control group,hypoxic injury potential(HIP) appeared in all slices during simulated ischemia,after reoxygenation the OPS recovered a little;ginsenoside Rb 1(600μmol/L) decreased the appearance of HIP,after reoxygenation,the recovery rate and amplitudes of OPS were significantly higher than those of the control group. (2)The effect of ginsenoside Rb 1 against the Glutamate excitory toxicity:in control group,Glutamate(1.5mmol/L) decreased the amplitude of OPS,after the end of Glutamate exposure,the recovery rate and amplitude of OPS were low;after administration of ginsenoside Rb 1(600μmol/L),the recovery rate and amplitude of OPS were significantly higher than those of the control group. Conclusion Ginsenoside Rb 1 has the protective effects against ischemic brain injury. The mechanism is related to the antagonist effect of ginsenosides on Glutamate excitory toxicity.