自噬在乙醇介导神经毒性中的保护作用及机制

The protective effects and mechanisms of autophagy on ethanol-mediated neurotoxicity

乙醇暴露能够导致神经元变性及神经元死亡,引起严重的神经系统损伤。发育期的神经系统对乙醇更为敏感,产前摄入乙醇可导致胎儿酒精谱系障碍;在成人中,慢性乙醇摄入可导致WernickeKorsakof f综合征等慢性酒精中毒性神经疾病。自噬作为对乙醇毒性的保护性机制,它能够缓解乙醇介导的神经元凋亡及其他病理性反应。乙醇通过多种细胞分子机制激活自噬,包括介导氧化应激、内质网应激、m TOR及AMPK信号通路等。本文总结讨论目前自噬参与乙醇神经毒性相关机制及研究进展。

Ethanol exposure can result in neuronal death and neuronal degeneration, which are severely detrimental to the brain. hTe developing brain is particularly vulnerable to ethanol such that prenatal ethanol consumption causes fetal alcohol spectrum disorders;and long-term ethanol intake can lead to chronic alcoholic nervous disease in adults such as Wernicke-Korsakoff syndrome. One cellular mechanism that acts as a protective response is autophagy, which can alleviate ethanol-induced neuron apoptosis and other pathological responses. Ethanol may stimulate autophagy through multiple mechanisms including induction of oxidative stress and endoplasmic reticulum stress, modulation of MTOR and AMPK signaling. hTis review summarizes and discusses the recent progress and mechanisms regarding the involvement of autophagy in ethanol-mediated neurotoxicity.