mptp治疗小鼠腹侧中脑和纹状体氧化应激和表观遗传修饰的动态变化:对帕金森病发病机制的影响

IF 2.9 3区 医学 Q2 NEUROSCIENCES
Pablo Gallo-Soljancic, Maria Egle De Stefano, Ana-Maria Gonzalez-Cuello, Emiliano Fernandez-Villalba, Lode Godderis, Maria Trinidad Herrero
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引用次数: 0

摘要

本研究探讨了急性1-metil - 4-fenil 1,2,3,6-四氢吡啶那(MPTP)治疗对小鼠腹侧中脑(VM)和纹状体氧化应激和表观遗传变化的影响,MPTP是一种已知的帕金森病诱导剂。在注射后4、8、24和48 h分析关键标志物:嘌呤鸟嘌呤的羟基化形式(8-羟基-2'-脱氧鸟苷;8-OHdG),氧化应激的标志;胞嘧啶的甲基化形式(5-甲基胞嘧啶;5-mC),与基因沉默相关;胞嘧啶的羟基甲基化形式(5-羟甲基胞嘧啶;5-hmC),参与去甲基化和基因调控。结果显示,VM中8-OHdG水平明显下降,表明氧化应激反应迅速,而纹状体表现出不太明显的反应,反映了氧化应激易感性的区域差异。DNA甲基化模式显示VM中5-mC水平的复杂和双相变化,与纹状体中不太明显的反应形成对比,表明甲基化稳态被破坏和区域表观遗传变异性。MPTP治疗也显著降低了VM中的5-hmC水平,表明活性DNA去甲基化受损和表观遗传灵活性受损。相反,纹状体持续保持高5-hmC水平,反映了该区域特有的代偿性羟甲基化机制。这些发现突出了氧化应激易感性和表观遗传调控的显著区域差异,VM对氧化损伤表现出更高的敏感性和受损的表观遗传灵活性。这强调了理解氧化和表观遗传机制在帕金森病病理生理中的作用的重要性,这些变化为针对氧化DNA损伤和表观遗传稳态的新治疗策略铺平了道路。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Dynamic Changes in Oxidative Stress and Epigenetic Modifications in the Ventral Mesencephalon and Striatum of MPTP-Treated Mice: Implications for Parkinson's Disease Pathogenesis.

This study investigates the effects of an acute 1-metil 4-fenil 1,2,3,6-tetraidro-piridina (MPTP) treatment, a known inducer of parkinsonism, on oxidative stress and epigenetic changes in the mouse ventral midbrain (VM) and striatum. Key markers were analyzed at 4, 8, 24, and 48 h post-injections: the hydroxylated form of the purine guanine (8-hydroxy-2'-deoxyguanosine; 8-OHdG), a marker of oxidative stress; the methylated form of cytosine (5-methylcytosine; 5-mC), associated with gene silencing; the hydroxy methylated form of cytosine (5-hydroxymethylcytosine; 5-hmC), involved in demethylation and gene regulation. The results showed a pronounced decrease in 8-OHdG levels in the VM, suggesting a rapid oxidative stress response, whereas the striatum exhibited a less pronounced response, reflecting regional differences in oxidative stress vulnerability DNA methylation patterns revealed complex and biphasic changes in 5-mC levels in the VM, contrasted with a less pronounced response in the striatum, suggesting disrupted methylation homeostasis and regional epigenetic variability. MPTP treatment also significantly reduced in 5-hmC levels in the VM, pointing to impaired active DNA demethylation and compromised epigenetic flexibility. In contrast, the striatum maintained consistently high 5-hmC levels, reflecting compensatory hydroxymethylation mechanisms specific to this region. These findings highlight pronounced regional differences in oxidative stress vulnerability and epigenetic regulation, with the VM showing heightened sensitivity to oxidative damage and impaired epigenetic flexibility. This underscores the importance of understanding the role of oxidative and epigenetic mechanisms in Parkinson's disease pathophysiology, The changes pave the way for novel therapeutic strategies targeting oxidative DNA damage and epigenetic homeostasis.

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来源期刊
Neurotoxicity Research
Neurotoxicity Research 医学-神经科学
CiteScore
7.70
自引率
5.40%
发文量
164
审稿时长
6-12 weeks
期刊介绍: Neurotoxicity Research is an international, interdisciplinary broad-based journal for reporting both basic and clinical research on classical neurotoxicity effects and mechanisms associated with neurodegeneration, necrosis, neuronal apoptosis, nerve regeneration, neurotrophin mechanisms, and topics related to these themes. Published papers have focused on: NEURODEGENERATION and INJURY Neuropathologies Neuronal apoptosis Neuronal necrosis Neural death processes (anatomical, histochemical, neurochemical) Neurodegenerative Disorders Neural Effects of Substances of Abuse NERVE REGENERATION and RESPONSES TO INJURY Neural Adaptations Neurotrophin mechanisms and actions NEURO(CYTO)TOXICITY PROCESSES and NEUROPROTECTION Excitatory amino acids Neurotoxins, endogenous and synthetic Reactive oxygen (nitrogen) species Neuroprotection by endogenous and exogenous agents Papers on related themes are welcome.
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