Ginsenoside Rb1 confers neuroprotection via promotion of glutamate transporters in a mouse model of Parkinson's disease.
Ginsenoside Rb1 confers neuroprotection via promotion of glutamate transporters in a mouse model of Parkinson's disease.
复制标题
人参皂苷 Rb1 通过促进帕金森病小鼠模型中的谷氨酸转运蛋白提供神经保护
DOI：
10.1016/j.neuropharm.2017.12.012
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发表时间：
2017
影响因子：
4.7
通讯作者：
Lei Wen
中科院分区：
文献类型：
--
作者：
Yun-Long Zhang;Yan Liu;Xin-Pan Kang;Chun-Yan Dou;Ren-Gong Zhuo;Shu-Qiong Huang;Li Peng;Lei Wen
人参皂甙Rb 1对体外培养的多巴胺能神经元有保护作用。然而，Rb 1在治疗帕金森病（PD）中的神经保护作用和潜在机制仍不清楚。本研究以1-甲基-4-苯基-1，2，3，6-四氢吡啶（MPTP）模型小鼠为研究对象，从神经递质传递和兴奋毒性两个方面探讨Rb 1对PD小鼠运动障碍的影响及其机制。在这里，我们首次报道了Rb 1治疗可改善MPTP小鼠PD模型的运动缺陷，防止DA神经元死亡，并抑制α-突触核蛋白表达和星形胶质细胞增生。rb 1通过上调谷氨酸转运蛋白的表达和功能，调节黑质纹状体和皮质-黑质多巴胺能传递途径，减弱谷氨酸兴奋性毒性。我们的研究结果表明，Rb 1通过核转位的核因子-κ B增加谷氨酸转运蛋白的表达，调节谷氨酸受体的表达，促进突触蛋白的表达。这些结果表明，Rb 1抑制谷氨酸兴奋毒性和调节突触传递，以改善运动功能的MPTP模型的PD的损害，这表明Rb 1可能作为一个潜在的治疗剂。
Ginsenoside Rb1 has been demonstrated to protect dopaminergic (DA) neurons from deathin vitro. However, the neuroprotective effects and underlying mechanism of Rb1 in treating Parkinson's disease (PD) remain uncharacterized. In this study, we explored the effects of Rb1 on the movement disorder and the underlying mechanisms based on the glutamatergic transmission and excitotoxicity in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD. Here, for the first time, we report that Rb1 treatment ameliorates motor deficits, prevents DA neuron death, and suppresses α-synuclein expression and astrogliosis in the MPTP mouse model of PD. Rb1 attenuates glutamate excitotoxicity by upregulating glutamate transporter expression and function, and modulating the nigrostriatal and cortico-nigral glutamatergic transmission pathways. Our results demonstrate that Rb1 increases glutamate transporter expression via nuclear translocation of nuclear factor-kappa B, regulates glutamate receptor expression and promotes synaptic protein expression. These results indicate that Rb1 suppresses glutamate excitotoxicity and modulates synaptic transmission to improve the impairments in motor functions of the MPTP model of PD, suggesting that Rb1 may serve as a potential therapeutic agent for PD.