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Brain Res. 2017 Dec 1;1676:83-90. doi: 10.1016/j.brainres.2017.09.013. Epub 2017 Sep 11.

Piracetam inhibits ethanol (EtOH)-induced memory deficit by mediating multiple pathways.

Author information

1
Department of Neurology, The Third People's Hospital of Chengdu, The Affiliated Hospital of Southwest Jiaotong University, Chengdu, Sichuan, China.
2
Department of Cardiology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, China.
3
Department of Rehabilitation, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, China. Electronic address: xufangyuan@swmu.edu.cn.
4
Department of Rehabilitation, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, China. Electronic address: wjl2015284@fmmu.edu.cn.

Abstract

Excessive ethanol (EtOH) intake, especially to prenatal exposure, can significantly affect cognitive function and cause permanent learning and memory injures in children. As a result, how to protect children from EtOH neurotoxicity has gained increasing attention in recent years. Piracetam (Pir) is a nootropic drug derived from c-aminobutyric acid and can manage cognition impairments in multiple neurological disorders. Studies have shown that Pir can exert therapeutic effects on EtOH-induced memory impairments, but the underlying mechanism is still unknown. In this study, we found that Pir inhibited ethanol-induced memory deficit by mediating multiple pathways. Treatment with EtOH could cause cognitive deficit in juvenile rats, and triggered the alteration of synaptic plasticity. Administration with Pir significantly increased long-term potentiation and protected hippocampus neurons from EtOH neurotoxicity. Pir intervention ameliorated EtOH-induced cell apoptosis and inhibited the activation of Caspase-3 in vitro, suggesting that Pir protected neurons by anti-apoptotic effects. Pir could decrease the expression of LC3-II and Beclin-1 induced by EtOH, and increase the phosphorylation of mTOR and reduce the phosphorylation of Akt, which suggested that the protective effect of Pir was involved in regulation of autophagic process and mTOR/Akt pathways. In conclusion, we speculate that Pir reduces EtOH-induced neuronal damage by regulation of apoptotic action and autophagic action, and our research offers preclinical evidence for the application of Pir in ethanol toxicity.

KEYWORDS:

Apoptosis; Autophagy; Ethanol; Hippocampus; Memory; Piracetam

PMID:
28912059
DOI:
10.1016/j.brainres.2017.09.013
[Indexed for MEDLINE]

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