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甲基苯丙胺诱导的神经元损伤:神经毒性与神经炎症

Methamphetamine-Induced Neuronal Damage: Neurotoxicity and Neuroinflammation.

作者信息

Kim Buyun, Yun Jangmi, Park Byoungduck

机构信息

College of Pharmacy, Keimyung University, Daegu 42601, Republic of Korea.

出版信息

Biomol Ther (Seoul). 2020 Sep 1;28(5):381-388. doi: 10.4062/biomolther.2020.044.

Abstract

Methamphetamine (METH) is a highly addictive psychostimulant and one of the most widely abused drugs worldwide. The continuous use of METH eventually leads to drug addiction and causes serious health complications, including attention deficit, memory loss and cognitive decline. These neurological complications are strongly associated with METH-induced neurotoxicity and neuroinflammation, which leads to neuronal cell death. The current review investigates the molecular mechanisms underlying METH-mediated neuronal damages. Our analysis demonstrates that the process of neuronal impairment by METH is closely related to oxidative stress, transcription factor activation, DNA damage, excitatory toxicity and various apoptosis pathways. Thus, we reach the conclusion here that METH-induced neuronal damages are attributed to the neurotoxic and neuroinflammatory effect of the drug. This review provides an insight into the mechanisms of METH addiction and contributes to the discovery of therapeutic targets on neurological impairment by METH abuse.

摘要

甲基苯丙胺(METH)是一种极易成瘾的精神兴奋剂,也是全球滥用最为广泛的毒品之一。持续使用METH最终会导致药物成瘾,并引发严重的健康并发症,包括注意力缺陷、记忆力丧失和认知能力下降。这些神经并发症与METH诱导的神经毒性和神经炎症密切相关,进而导致神经元细胞死亡。本综述研究了METH介导的神经元损伤的分子机制。我们的分析表明,METH导致神经元损伤的过程与氧化应激、转录因子激活、DNA损伤、兴奋性毒性和各种凋亡途径密切相关。因此,我们在此得出结论,METH诱导的神经元损伤归因于该药物的神经毒性和神经炎症作用。本综述深入探讨了METH成瘾的机制,并有助于发现针对METH滥用所致神经损伤的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4430/7457172/3a32ead61cf1/BT-28-381-f1.jpg

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