Effects of Panax notoginseng ginsenoside Rb1 on abnormal hippocampal microenvironment in rats.
Effects of Panax notoginseng ginsenoside Rb1 on abnormal hippocampal microenvironment in rats.
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DOI：
10.1016/j.jep.2017.01.005
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发表时间：
2017-04
影响因子：
5.4
通讯作者：
Shiyun Wang;Minghong Li;Ying Guo;Chen Li;Lanou Wu;Xin-Fu Zhou;Yaohui Luo;D. An;Shude Li;Haiyun Luo;Lijin Pu
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文献类型：
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作者：
Shiyun Wang;Minghong Li;Ying Guo;Chen Li;Lanou Wu;Xin-Fu Zhou;Yaohui Luo;D. An;Shude Li;Haiyun Luo;Lijin Pu
脑缺血对中枢神经元造成损伤，缺血微环境的异常是导致损伤的关键因素。局部谷氨酸浓度升高、Ca ~（2+）超载、细胞色素C释放引起的线粒体应激是脑缺血微环境异常的重要因素。本研究采用两种动物模型（微灌流模型和光血栓模型），应用三七皂苷Rb 1干预海马CA 1区神经元的异常环境。结果：与假手术组相比，黄芪具有以下作用。a）在两种模型中，Rb 1均能增加海马CA 1区局部脑血流量（rCBF），增加神经元超微结构的稳定性，改善神经元的适应性。B）Rb 1可提高缺血后胶质细胞谷氨酸转运体1（GLT-1）的表达水平，逆转缺血后谷氨酸（Glu）的摄取，从而降低Glu的兴奋性，且GLT-1的表达水平与Rb 1的剂量成正比，与尼莫地平相似。c）NMDAR表达水平降低，Ca ~（2+）超载，减轻神经元损伤。NMDAR的表达水平与尼莫地平的作用相似，与NMDRb 1的剂量成反比。d）Rb 1能减少细胞色素C（Cyt-C）的释放，减轻神经元线粒体应激引起的损伤。同时，Cyt-C的释放量与尼莫地平的释放量相似，但与剂量成反比。人参皂苷Rb 1可能作为一种有效的神经保护药物，改善急性脑缺血后的脑血流量，预防脑卒中继发性脑损伤。
Cerebral ischemia damages central neurons, and abnormal microenvironment in ischemic condition is the key factor to the damages. The increase of local concentration of glutamic acid, the overload of Ca2+, and the mitochondrial stress caused by release of cytochrome C are important factors of abnormal microenvironment in cerebral ischemia. In this study ginsenoside Rb1, a compound from Panax Notoginseng, was used to intervene abnormal environment of neurons in the hippocampal CA1 region in two animal models (microperfusion model and photothrombosis model). Results: Compared with the vehicle in the sham group, ginsenoside had following effects. a) ginsenoside Rb1 increased the regional cerebral blood flow (rCBF) and the stability of neuronal ultrastructure in in the hippocampal CA1 region and improved the adaptability of neurons in two models. b) ginsenoside Rb1 improved the expression level of glial glutamate transporter1 (GLT-1) and reversed the uptake of glutamate (Glu) after ischemia, and as a result thereby decreased the excitability of Glu and the expression level of GLT-1 was proportional to the dose of ginsenoside Rb1 and similar to that of Nimodipine. c) ginsenoside Rb1 inhibited the expression level of NMDAR and the overload of Ca2+, thereby reducing neuronal damages. Meanwhile, the expression level of NMDAR was inversely proportional to the dose of ginsenoside Rb1, which was similar to that of Nimodipine. d) ginsenoside Rb1 decreased the release of cytochrome C (Cyt-C) and reduced the damages caused by neuronal mitochondrial stress. Meanwhile, the release of Cyt-C was inversely proportional to the dose of ginsenoside Rb1, which was similar to that of Nimodipine. Ginsenoside Rb1 may be as an effective drug for neuroprotection and improve cerebral blood flow after acute ischemia and prevent the secondary brain damage induced by stroke.