Neuroprotective effect of ginsenoside Rb1 on glutamate-induced neurotoxicity: With emphasis on autophagy
Neuroprotective effect of ginsenoside Rb1 on glutamate-induced neurotoxicity: With emphasis on autophagy
复制标题
人参皂苷 Rb1 对谷氨酸诱导的神经毒性的神经保护作用：重点是自噬
DOI：
10.1016/j.neulet.2010.07.052
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发表时间：
2010-10-04
影响因子：
2.5
通讯作者：
Xu, Gelin
中科院分区：
文献类型：
--
作者：
Chen, Zhaoyao;Lu, Tingting;Xu, Gelin
人参皂苷Rb 1已被证明具有神经保护作用，但其机制尚不清楚。本研究旨在探讨抗谷氨酸受体Rb 1对谷氨酸损伤神经元自噬激活的影响及其机制。将指数浓度（1.2、12、120 μ M）的人参皂苷Rb 1或自噬抑制剂3-甲基腺嘌呤（5 mM）加入到用谷氨酸处理后的皮层神经元的培养基中。通过MU测定测量细胞活力。透射电镜观察自噬体形成。自噬标记蛋白LC 3用免疫荧光法检测，并在激光共聚焦显微镜下观察。Western blot检测自噬相关蛋白Beclin-1的变化。我们发现，TRB 1保护皮层神经元免受谷氨酸诱导的细胞损伤。谷氨酸处理后，自噬被激活，与对照相比，自噬体和点状LC 3均显著增加。Beclin-1在谷氨酸处理的细胞中升高。自噬体和点状LC 3的形成被抑制Rb 1。Beclin-1的水平，同时降低与谷氨酸处理的细胞相比，Beclin-1处理的细胞。这些结果表明，自噬的抑制可能是负责谷氨酸诱导的损伤的神经保护作用的cDNARb 1。Beclin-1的下调可能在这一过程中发挥重要作用。(C)2010爱思唯尔爱尔兰有限公司版权所有。
Ginsenoside Rb1 has been demonstrated with neuroprotective effects, but the mechanisms remain unclear. This study aimed to probe the effects and mechanisms of ginsenoside Rb1 on activation of autophagy in glutamate-injured neurons. Ginsenoside Rb1 of exponential concentrations (1.2, 12, 120 mu M) or autophagy inhibitor 3-methyladenine (5 mM) was added to culture medium for cortical neurons after being treated with glutamate. Cell viability was measured by MU assay. Autophagosomes formation was observed with transmission electron microscope. Autophagy marked protein LC3 was detected with immunofluorescence and visualized under laser confocal microscopy. Changes of autophagy related protein Beclin-1 were measured with Western blot. We found that ginsenoside Rb1 protected cortical neurons from glutamate-induced cell injury. Autophagy was activated after glutamate treatment, with both autophagosomes and punctate LC3 increased significantly compared with control. Beclin-1 was elevated in glutamate-treated cells. Formation of autophagosome and punctate LC3 was attenuated by ginsenoside Rb1. The level of Beclin-1 in ginsenoside Rb1 treated cells was simultaneously decreased compared with glutamate-treated cells. These results suggested that inhibition of autophagy could be responsible for neuroprotective effects of ginsenoside Rb1 in glutamate-induced injury. Down-regulation of Beclin-1 may play an important role in this process. (C) 2010 Elsevier Ireland Ltd. All rights reserved.