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首页> 美国卫生研究院文献>Therapeutic Advances in Endocrinology and Metabolism >Ghrelin is neuroprotective in Parkinson’s disease: molecular mechanisms of metabolic neuroprotection
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Ghrelin is neuroprotective in Parkinson’s disease: molecular mechanisms of metabolic neuroprotection

机译：Ghrelin对帕金森氏病具有神经保护作用：代谢性神经保护作用的分子机制

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Ghrelin is a circulating orexigenic signal that rises with prolonged fasting and falls postprandially. Ghrelin regulates energy homeostasis by stimulating appetite and body weight; however, it also has many nonmetabolic functions including enhanced learning and memory, anxiolytic effects as well as being neuroprotective. In Parkinson’s disease, ghrelin enhances dopaminergic survival via reduced microglial and caspase activation and improved mitochondrial function. As mitochondrial dysfunction contributes to Parkinson’s disease, any agent that enhances mitochondrial function could be a potential therapeutic target. We propose that ghrelin provides neuroprotective effects via AMPK (5′ adenosine monophosphate-activated protein kinase) activation and enhanced mitophagy (removal of damaged mitochondria) to ultimately enhance mitochondrial bioenergetics. AMPK activation shifts energy balance from a negative to a neutral state and has a role in regulating mitochondrial biogenesis and reducing reactive oxygen species production. Mitophagy is important in Parkinson’s disease because damaged mitochondria produce reactive oxygen species resulting in damage to intracellular proteins, lipids and DNA predisposing them to neurodegeneration. Many genetic mutations linked to Parkinson’s disease are due to abnormal mitochondrial function and mitophagy, for example LRRK2, PINK1 and Parkin. An interaction between ghrelin and these classic Parkinson’s disease markers has not been observed, however by enhancing mitochondrial function, ghrelin or AMPK is a potential therapeutic target for slowing the progression of Parkinson’s disease symptoms, both motor and nonmotor.
机译：Ghrelin是一种循环的致病信号，随着禁食时间的延长而上升，并在餐后下降。 Ghrelin通过刺激食欲和体重来调节能量稳态。然而，它也具有许多非代谢功能，包括增强的学习和记忆，抗焦虑作用以及神经保护作用。在帕金森氏病中，生长素释放肽通过减少小胶质细胞和caspase的活化以及改善线粒体功能来提高多巴胺能生存。由于线粒体功能障碍是帕金森氏症的病因，任何增强线粒体功能的药物都可能成为潜在的治疗靶标。我们建议ghrelin通过AMPK（5'腺苷单磷酸激活蛋白激酶）激活和增强线粒体（去除受损的线粒体）提供神经保护作用，从而最终增强线粒体的生物能。 AMPK激活将能量平衡从负态变为中性，并在调节线粒体生物发生和减少活性氧产生中发挥作用。线粒体在帕金森氏病中很重要，因为受损的线粒体会产生活性氧，从而导致细胞内蛋白质，脂质和DNA受损，使它们容易发生神经变性。与帕金森氏病有关的许多基因突变是由于线粒体功能异常和线粒体突变所致，例如LRRK2，PINK1和帕金森氏病。 ghrelin与这些经典的帕金森氏病标志物之间尚未发现相互作用，但是通过增强线粒体功能，ghrelin或AMPK是减缓帕金森氏病症状（运动和非运动）进展的潜在治疗靶标。

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