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用于帕金森病研究的脂多糖小鼠模型:批判性评价

Lipopolysaccharide mouse models for Parkinson's disease research: a critical appraisal.

作者信息

Deng Isaac, Bobrovskaya Larisa

机构信息

Health and Biomedical Innovation, Clinical and Health Sciences, University of South Australia, Adelaide, Australia.

出版信息

Neural Regen Res. 2022 Nov;17(11):2413-2417. doi: 10.4103/1673-5374.331866.

DOI:10.4103/1673-5374.331866
PMID:35535880
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9120679/
Abstract

Parkinson's disease, the most common movement disorder, has a strong neuroinflammatory aspect. This is evident by increased pro-inflammatory cytokines in the serum, and the presence of activated microglial cells, and inflammatory cytokines in the substantia nigra of post-mortem brains as well as cerebrospinal fluid of Parkinson's disease patients. The central and peripheral neuroinflammatory aspects of Parkinson's disease can be investigated in vivo via administration of the inflammagen lipopolysaccharide, a component of the cell wall of gram-negative bacteria. In this mini-review, we will critically evaluate different routes of lipopolysaccharide administration (including intranasal systemic and stereotasic), their relevance to clinical Parkinson's disease as well as the recent findings in lipopolysaccharide mouse models. We will also share our own experiences with systemic and intrastriatal lipopolysaccharide models in C57BL/6 mice and will discuss the usefulness of lipopolysaccharide mouse models for future research in the field.

摘要

帕金森病是最常见的运动障碍疾病,具有很强的神经炎症特征。血清中促炎细胞因子增加、死后大脑黑质以及帕金森病患者脑脊液中存在活化的小胶质细胞和炎性细胞因子,都证明了这一点。帕金森病的中枢和外周神经炎症特征可通过给予炎性介质脂多糖(革兰氏阴性菌细胞壁的一种成分)在体内进行研究。在这篇小型综述中,我们将批判性地评估脂多糖的不同给药途径(包括鼻内、全身和立体定向给药)、它们与临床帕金森病的相关性以及脂多糖小鼠模型的最新研究结果。我们还将分享我们在C57BL/6小鼠中建立全身和纹状体内脂多糖模型的经验,并讨论脂多糖小鼠模型在该领域未来研究中的实用性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14da/9120679/4f8461902b0f/NRR-17-2413-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14da/9120679/4f8461902b0f/NRR-17-2413-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14da/9120679/4f8461902b0f/NRR-17-2413-g001.jpg

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本文引用的文献

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J Neuroinflammation. 2021 Oct 11;18(1):225. doi: 10.1186/s12974-021-02280-2.
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Lipopolysaccharide animal models of Parkinson's disease: Recent progress and relevance to clinical disease.帕金森病的脂多糖动物模型:最新进展及其与临床疾病的相关性
Brain Behav Immun Health. 2020 Mar 18;4:100060. doi: 10.1016/j.bbih.2020.100060. eCollection 2020 Apr.
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Low molecular weight polysialic acid prevents lipopolysaccharide-induced inflammatory dopaminergic neurodegeneration in humanized SIGLEC11 transgenic mice.
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Neural Regen Res. 2024 Sep 1;19(9):2081-2088. doi: 10.4103/1673-5374.391191. Epub 2024 Jan 12.
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Lipopolysaccharide-Induced Model of Neuroinflammation: Mechanisms of Action, Research Application and Future Directions for Its Use.脂多糖诱导的神经炎症模型:作用机制、研究应用及其未来应用方向。
Molecules. 2022 Aug 26;27(17):5481. doi: 10.3390/molecules27175481.
低相对分子质量聚唾液酸可预防人源化 SIGLEC11 转基因小鼠脂多糖诱导的炎症性多巴胺能神经退行性变。
Glia. 2021 Dec;69(12):2845-2862. doi: 10.1002/glia.24073. Epub 2021 Aug 18.
4
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Int J Mol Sci. 2021 Jul 9;22(14):7380. doi: 10.3390/ijms22147380.
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