褪黑素
冰毒-
神经毒性
甲基苯丙胺
氧化应激
神经炎症
神经退行性变
神经发生
药理学
活性氧
自噬
程序性细胞死亡
小胶质细胞
化学
炎症
生物
细胞生物学
医学
细胞凋亡
内分泌学
生物化学
内科学
免疫学
毒性
单体
有机化学
疾病
丙烯酸酯
聚合物
作者
Pawaris Wongprayoon,Piyarat Govitrapong
标识
DOI:10.2174/1381612822666151214125657
摘要
Methamphetamine (METH), an illegal psycho-stimulant, is widely known as a recreational drug. In addition to its addictive effect, METH induces neurotoxicity via multiple mechanisms. The major contributors to METH-induced neurotoxicity are reactive oxygen species, which lead to cell death through apoptotic pathway and disturbances in mitochondria, the generation of neuroinflammation, and autophagy. Melatonin, a neurohormone secreted by the pineal gland, is a potent antioxidant compound that plays a beneficial role by protecting against the oxidative stress caused by METH. Melatonin also plays a role in maintaining mitochondrial homeostasis. Nanomolar concentrations of melatonin have been shown to protect against the inflammation caused by METH and to prevent the decrease in neurogenesis caused by METH in progenitor cells obtained from adult rat hippocampal tissue. The intent of this review is to describe the underlying mechanisms involving melatonin that protect against the neurodegeneration caused by METH.
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