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锂通过调节糖原合酶激酶-3β活性缓解实验性自身免疫性神经炎大鼠的瘫痪。

Lithium alleviates paralysis in experimental autoimmune neuritis in Lewis rats by modulating glycogen synthase kinase-3β activity.

机构信息

Department of Animal Science, College of Life Science, Sangji University, Wonju 26339, Korea.

出版信息

J Vet Sci. 2024 Sep;25(5):e69. doi: 10.4142/jvs.24212.

DOI:10.4142/jvs.24212
PMID:39363657
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11450387/
Abstract

IMPORTANCE

Guillain-Barré syndrome (GBS)-like neuropathy mimics the leading cause of sporadic acute nontraumatic limb paralysis in individuals from developed countries. Experimental autoimmune neuritis (EAN) is an animal model of GBS and of syndromes such as acute canine polyradiculoneuritis, seen in dogs and cats.

OBJECTIVE

The involvement of glycogen synthase kinase (GSK)-3β, a pro-inflammatory molecule, in rat EAN is not fully understood. This study evaluated the potential role of GSK-3β in EAN through its inhibition by lithium.

METHODS

Lewis rats were injected with SP26 antigen to induce EAN. Lithium was administered from 1 day before immunization to day 14 post-immunization (PI). Then the rats were euthanized and their neural tissues were prepared for histological and Western blotting analyses.

RESULTS

Lithium, an inhibitor of GSK-3, significantly ameliorated EAN paralysis in rats, when administered from day 1 to day 14 PI. This corresponded with reduced inflammation in the sciatic nerves of EAN rats, where phosphorylation of GSK-3β was also upregulated, indicating suppression of GSK-3.

CONCLUSIONS AND RELEVANCE

These findings suggest that lithium, an inhibitor of GSK-3β, plays a significant role in ameliorating rat EAN paralysis, by suppressing GSK-3β and its related signals in EAN-affected sciatic nerves.

摘要

重要性

格林-巴利综合征(GBS)样神经病模仿了发达国家个体中散发性急性非创伤性肢体麻痹的主要原因。实验性自身免疫性神经炎(EAN)是 GBS 以及急性犬多发性神经根神经炎等综合征的动物模型,在犬和猫中可见到这种疾病。

目的

糖原合成酶激酶(GSK)-3β作为一种促炎分子,其在大鼠 EAN 中的作用尚未完全阐明。本研究通过锂抑制作用来评估 GSK-3β在 EAN 中的潜在作用。

方法

用 SP26 抗原对刘易斯大鼠进行免疫注射以诱导 EAN。从免疫前 1 天到免疫后 14 天(PI)给予锂治疗。然后处死大鼠,准备其神经组织进行组织学和 Western blot 分析。

结果

GSK-3 的抑制剂锂从 PI 第 1 天至第 14 天给药时,可显著改善 EAN 大鼠的瘫痪。这与 EAN 大鼠坐骨神经中的炎症减少相对应,其中 GSK-3β的磷酸化也上调,表明 GSK-3 的抑制。

结论和相关性

这些发现表明,GSK-3β抑制剂锂通过抑制 EAN 受累坐骨神经中的 GSK-3β及其相关信号,在改善大鼠 EAN 瘫痪方面发挥重要作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1747/11450387/b81b8c7a7664/jvs-25-e69-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1747/11450387/f22063d96aa0/jvs-25-e69-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1747/11450387/4b9e7c9cbc36/jvs-25-e69-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1747/11450387/aff54141c292/jvs-25-e69-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1747/11450387/2d069e9549a5/jvs-25-e69-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1747/11450387/b81b8c7a7664/jvs-25-e69-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1747/11450387/f22063d96aa0/jvs-25-e69-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1747/11450387/4b9e7c9cbc36/jvs-25-e69-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1747/11450387/aff54141c292/jvs-25-e69-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1747/11450387/2d069e9549a5/jvs-25-e69-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1747/11450387/b81b8c7a7664/jvs-25-e69-g005.jpg

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本文引用的文献

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Cell Mol Biol Lett. 2024 Jul 8;29(1):100. doi: 10.1186/s11658-024-00614-5.
2
CaMKK2 alleviates myocardial ischemia/reperfusion injury by inhibiting oxidative stress and inflammation via the action on the AMPK-AKT-GSK-3β/Nrf2 signaling cascade.钙调蛋白激酶激酶 2 通过作用于 AMPK-AKT-GSK-3β/Nrf2 信号级联来抑制氧化应激和炎症,从而减轻心肌缺血/再灌注损伤。
Inflamm Res. 2023 Jul;72(7):1409-1425. doi: 10.1007/s00011-023-01756-6. Epub 2023 Jun 20.
3
Zoonotic Transmission of to Caretakers From Sick Pen Calves Carrying a Mixed Population of Strains With and Without Guillain Barré Syndrome-Associated Lipooligosaccharide Loci.
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Front Microbiol. 2022 Apr 29;13:800269. doi: 10.3389/fmicb.2022.800269. eCollection 2022.
4
Guillain-Barré syndrome.格林-巴利综合征。
Lancet. 2021 Mar 27;397(10280):1214-1228. doi: 10.1016/S0140-6736(21)00517-1. Epub 2021 Feb 26.
5
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Biomed Pharmacother. 2020 Dec;132:110874. doi: 10.1016/j.biopha.2020.110874. Epub 2020 Oct 18.
6
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J Neurol. 2021 Oct;268(10):3728-3743. doi: 10.1007/s00415-020-10034-y. Epub 2020 Jun 30.
7
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9
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