지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
커뮤니티
연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2024.9
- 수록면
- 106 - 115 (10page)
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초록· 키워드
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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.
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.
목차
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
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