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神经退行性疾病中氧化应激和炎症反应的新见解

New Insights into Oxidative Stress and Inflammatory Response in Neurodegenerative Diseases.

作者信息

Scarian Eveljn, Viola Camilla, Dragoni Francesca, Di Gerlando Rosalinda, Rizzo Bartolo, Diamanti Luca, Gagliardi Stella, Bordoni Matteo, Pansarasa Orietta

机构信息

Cellular Models and Neuroepigenetics Unit, IRCCS Mondino Foundation, Via Mondino 2, 27100 Pavia, Italy.

Department of Brain and Behavioral Sciences, University of Pavia, Via Agostino Bassi 21, 27100 Pavia, Italy.

出版信息

Int J Mol Sci. 2024 Feb 26;25(5):2698. doi: 10.3390/ijms25052698.

DOI:10.3390/ijms25052698
PMID:38473944
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10931808/
Abstract

Oxidative stress (OS) and inflammation are two important and well-studied pathological hallmarks of neurodegenerative diseases (NDDs). Due to elevated oxygen consumption, the high presence of easily oxidizable polyunsaturated fatty acids and the weak antioxidant defenses, the brain is particularly vulnerable to oxidative injury. Uncertainty exists over whether these deficits contribute to the development of NDDs or are solely a consequence of neuronal degeneration. Furthermore, these two pathological hallmarks are linked, and it is known that OS can affect the inflammatory response. In this review, we will overview the last findings about these two pathways in the principal NDDs. Moreover, we will focus more in depth on amyotrophic lateral sclerosis (ALS) to understand how anti-inflammatory and antioxidants drugs have been used for the treatment of this still incurable motor neuron (MN) disease. Finally, we will analyze the principal past and actual clinical trials and the future perspectives in the study of these two pathological mechanisms.

摘要

氧化应激(OS)和炎症是神经退行性疾病(NDDs)两个重要且研究充分的病理特征。由于耗氧量增加、易氧化的多不饱和脂肪酸大量存在以及抗氧化防御能力薄弱,大脑特别容易受到氧化损伤。这些缺陷是导致神经退行性疾病发展的原因,还是仅仅是神经元变性的结果,目前尚不确定。此外,这两个病理特征相互关联,已知氧化应激会影响炎症反应。在这篇综述中,我们将概述主要神经退行性疾病中这两条途径的最新研究结果。此外,我们将更深入地关注肌萎缩侧索硬化症(ALS),以了解抗炎和抗氧化药物如何用于治疗这种仍无法治愈的运动神经元(MN)疾病。最后,我们将分析这两种病理机制研究中过去和目前的主要临床试验以及未来展望。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2298/10931808/5a71460cd65a/ijms-25-02698-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2298/10931808/48d07c8e7e32/ijms-25-02698-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2298/10931808/5a71460cd65a/ijms-25-02698-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2298/10931808/48d07c8e7e32/ijms-25-02698-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2298/10931808/5a71460cd65a/ijms-25-02698-g002.jpg

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1
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2
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Int J Mol Sci. 2023 Feb 13;24(4):3739. doi: 10.3390/ijms24043739.
3
Epidemiology of neurodegenerative diseases in the East African region: A meta-analysis.
脑巨噬细胞和软脑膜成纤维细胞在髓鞘形成不足模型中促进炎症反应。
Acta Neuropathol Commun. 2025 Jul 4;13(1):145. doi: 10.1186/s40478-025-02063-3.
4
Annexin A5 ameliorates HO-induced cytotoxicity in SH-SY5Y cells.膜联蛋白A5可改善HO诱导的SH-SY5Y细胞的细胞毒性。
Mol Biol Rep. 2025 Jun 29;52(1):653. doi: 10.1007/s11033-025-10726-6.
5
The rise of 3D bioprinting advancements in modeling neurodegenerative diseases.3D生物打印技术在神经退行性疾病建模方面的进展兴起。
Ibrain. 2025 Apr 22;11(2):259-267. doi: 10.1002/ibra.12196. eCollection 2025 Summer.
6
Silicon-enriched meat consumption mitigates brain cortex damage associated with diabetic dyslipidemia in a late-stage type 2 diabetes mellitus rat model.在晚期2型糖尿病大鼠模型中,食用富含硅的肉类可减轻与糖尿病血脂异常相关的大脑皮质损伤。
Redox Biol. 2025 May 31;85:103697. doi: 10.1016/j.redox.2025.103697.
7
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Antioxidants (Basel). 2025 May 9;14(5):568. doi: 10.3390/antiox14050568.
8
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9
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Inflammation. 2025 Apr 16. doi: 10.1007/s10753-025-02301-9.
东非地区神经退行性疾病的流行病学:一项荟萃分析。
Front Neurol. 2022 Nov 17;13:1024004. doi: 10.3389/fneur.2022.1024004. eCollection 2022.
4
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Oxid Med Cell Longev. 2022 Oct 19;2022:1225578. doi: 10.1155/2022/1225578. eCollection 2022.
5
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Antioxidants (Basel). 2022 Sep 25;11(10):1897. doi: 10.3390/antiox11101897.
6
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7
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8
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Int J Mol Sci. 2022 May 25;23(11):5938. doi: 10.3390/ijms23115938.
9
Medications on hypertension, hyperlipidemia, diabetes, and risk of amyotrophic lateral sclerosis: a systematic review and meta-analysis.高血压、高血脂、糖尿病药物与肌萎缩侧索硬化症风险的关系:系统评价和荟萃分析。
Neurol Sci. 2022 Sep;43(9):5189-5199. doi: 10.1007/s10072-022-06131-7. Epub 2022 May 26.
10
Neuronal Hyperexcitability and Free Radical Toxicity in Amyotrophic Lateral Sclerosis: Established and Future Targets.肌萎缩侧索硬化症中的神经元过度兴奋和自由基毒性:既定靶点与未来靶点
Pharmaceuticals (Basel). 2022 Mar 31;15(4):433. doi: 10.3390/ph15040433.