Evidence map›Paper›PMID 39363657›Full record

ArticleJournal of veterinary science2024

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

Meejung Ahn

Abstract read
In one paragraph

Article in Journal of veterinary science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

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5 · Who and what money

Authors and funding

1 author.

Meejung AhnDepartment of Animal Science, College of Life Science, Sangji University, Wonju 26339, Korea. meeahn20@sangji.ac.kr.ORCID https://orcid.org/0000-0002-7302-9694

Funding

National Research Foundation of Korea NRF-2021M3H9A1097596Sangji University
6 · The paper itself

Abstract

importanceGuillain-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.

objectiveThe 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.

methodsLewis 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.

resultsLithium, 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.

Indexed as

Glycogen Synthase Kinase 3 betaNeuritis, Autoimmune, ExperimentalRats, Inbred LewAnimalsLithiumMaleParalysisRatsSciatic NerveGlycogen Synthase Kinase 3 betaLithiumExperimental autoimmune neuritisGSK-3lithiumsciatic nerve

Identifiers

PMID39363657
PMCPMC11450387

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.