Polysaccharide alleviates neurodegeneration and behavioral deficit by enhancing mitochondrial autophagy in chronic methamphetamine mice

IF 3.4 3区医学 Q2 NEUROSCIENCES

Neurotoxicology Pub Date : 2025-02-14 DOI:10.1016/j.neuro.2025.02.004

Han Yang , Yuanhe Wang , Shan Liu , Shan Zhang , Yuemeng Chen , Jiuyang Ding , Shunqin Chen , Faze Zhu , Bing Xia , Peng Luo , Yubo Liu

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引用次数: 0

Abstract

Methamphetamine (METH) is a psychostimulant drug widely abused because of its addictive properties.Its impact on the central nervous system is a major area of interest due to its unique ability to cross the blood-brain barrier, facilitated by its dual water and lipid solubility. Studies have indicated that oxidative stress, neuroinflammation, neuronal apoptosis, and mitochondrial dysfunction are primary mechanisms of METH-induced neurotoxicity. Mitophagy, a process regulated by the phosphatase and tensin homolog deleted on chromosome 10 (PTEN) induced kinase 1 (PINK1)/Parkin signaling pathway, has emerged as a critical mechanism for preserving mitochondrial function. Polysaccharides derived from bamboo fungus have shown potential in mitigating neurotoxicity. However, the role of these polysaccharides in ameliorating methamphetamine-induced neurotoxicity remains unclear. This study aimed to investigate whether polysaccharides could alleviate neurodegeneration in a chronic METH mice model and elucidate the underlying mechanisms and elucidate the mechanisms underlying METH-induced neuronal damage.

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多糖通过增强慢性甲基苯丙胺小鼠线粒体自噬来减轻神经变性和行为缺陷。

甲基苯丙胺（Methamphetamine，冰毒）是一种精神兴奋剂，因其成瘾性而被广泛滥用。它对中枢神经系统的影响是一个重要的研究领域，因为它具有独特的穿越血脑屏障的能力，这得益于它在水和脂质的双重溶解性。研究表明，氧化应激、神经炎症、神经元凋亡和线粒体功能障碍是甲基苯丙胺诱导的神经毒性的主要机制。线粒体自噬是由10号染色体上缺失的磷酸酶和紧张素同源物（PTEN）诱导的激酶1 (PINK1)/Parkin信号通路调节的过程，已成为保持线粒体功能的关键机制。从竹真菌中提取的多糖已显示出减轻神经毒性的潜力。然而，这些多糖在改善甲基苯丙胺诱导的神经毒性中的作用仍不清楚。本研究旨在探讨多糖是否可以减轻慢性冰毒小鼠模型的神经退行性变，并阐明其潜在机制，阐明冰毒诱导的神经元损伤机制。关键词:多糖;甲基苯丙胺;神经退化;线粒体自噬;法医毒理学。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Neurotoxicology 医学-毒理学

CiteScore

6.80

自引率

5.90%

发文量

161

审稿时长

70 days

期刊介绍： NeuroToxicology specializes in publishing the best peer-reviewed original research papers dealing with the effects of toxic substances on the nervous system of humans and experimental animals of all ages. The Journal emphasizes papers dealing with the neurotoxic effects of environmentally significant chemical hazards, manufactured drugs and naturally occurring compounds.