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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >ALCAR promote adult hippocampal neurogenesis by regulating cell-survival and cell death-related signals in rat model of Parkinson's disease like-phenotypes
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ALCAR promote adult hippocampal neurogenesis by regulating cell-survival and cell death-related signals in rat model of Parkinson's disease like-phenotypes

机译：Alcar通过调节帕金森病等表型的大鼠模型中的细胞存活和细胞死亡相关信号来促进成人海马神经发生

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Parkinson's disease (PD) is characterized by the degeneration of dopaminergic neurons in the nigrostriatal pathway that leading to progressive motor and nonmotor symptoms. The formation of newborn neurons in the adult hippocampus is affected by many factors such as anxiety, depression and impairment in learning and memory that are commonly observed nonmotor symptoms in PD, indicating the role of adult neurogenesis in PD pathophysiology. Acetyl-L-carnitine (ALCAR), regulate mitochondrial metabolism and has been reported to improve cognitive functions in different neurodegenerative disorders through an unknown mechanism. For the first time, we investigated the effect of ALCAR on adult neurogenesis in the 6-hydroxydopamine (6-OHDA) induced rat model of PD-like phenotypes and also explored the possible underlying mechanism of action. A single unilateral administration of 6-OHDA into the medial forebrain bundle reduced neural progenitor cell (NPC) proliferation, long-term survival and neuronal differentiation in the hippocampus. Interestingly, chronic treatment with ALCAR (100 mg/kg/ day, i.p) potentially enhanced proliferation, long term survival and neuronal differentiation of NPCs in rat model of PD-like phenotypes. ALCAR treatment stimulates cell survival related signals (AICT and BCL-2) by inhibiting cell death related cues (GSK-3 beta and BAX) which might be responsible for a neuroprotective effect of ALCAR in rat model of PD-like phenotypes. We conclude that ALCAR exerts neuroprotective effects against 6-OHDA-induced impairment in hippocampal neurogenesis by regulating cell survival and cell death-related signals. (C) 2017 Published by Elsevier Ltd.
机译：帕金森病（PD）的特征在于尼格塞尔途径中多巴胺能神经元的变性，导致渐进式电机和非运动症状。成年海马新生神经元的形成受许多因素的影响，如焦虑，抑郁和学习和记忆障碍，这些因素通常观察到PD中的非等症状，表明成人神经发生在Pd病理生理学中的作用。乙酰-1-肉碱（Alcar），调节线粒体代谢，并据报道，通过未知机制改善不同神经变性障碍中的认知功能。我们首次调查了Alcar对6-羟基多胺（6-OHDA）诱导的PD样表型大鼠模型中成年神经发生的影响，并探讨了可能的行动潜在机制。单个单侧施用6-OHDA进入内侧前脑束的缩减神经祖细胞（NPC）增殖，长期存活和海马的神经元分化。有趣的是，慢性治疗Alcar（100mg / kg /天，i.p）在Pd样表型的大鼠模型中潜在地增强了NPC的扩散，长期存活和神经元分化。 Alcar治疗通过抑制细胞死亡相关提示（GSK-3β和BAX）刺激细胞存活相关信号（AICT和BCL-2），这可能负责Alcar在大鼠Pd样表型的大鼠模型中的神经保护作用。我们得出结论，通过调节细胞存活和细胞死亡相关信号，Alcar对海马神经发生的6-OHDA诱导的损伤产生了神经保护作用。 （c）2017年由elestvier有限公司出版

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