The therapeutic effects of ginkgolides in Guillain-Barré syndrome and experimental autoimmune neuritis.


Journal

Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
ISSN: 1532-2653
Titre abrégé: J Clin Neurosci
Pays: Scotland
ID NLM: 9433352

Informations de publication

Date de publication:
May 2021
Historique:
received: 05 06 2020
revised: 14 12 2020
accepted: 15 02 2021
entrez: 17 4 2021
pubmed: 18 4 2021
medline: 23 6 2021
Statut: ppublish

Résumé

Guillain-Barré syndrome (GBS) is an acquired immune-mediated inflammatory peripheral neuropathy. The immune regulation of ginkgolides have been revealed in recent years. We herein investigate the potential therapeutic effects of ginkgolides both on GBS and its animal model, experimental autoimmune neuritis (EAN). EAN in C57BL/6 mice induced by subcutaneous injection with peripheral nerve myelin P0 protein peptide 180-199 (P0 peptide) were treated with ginkgolides at three different doses. GBS patients were randomly divided into two groups, the experimental group and the control group. The experimental group were treated with ginkgolides as soon as diagnosed. Our data indicated that ginkgolides administration daily ameliorated the score of EAN and delayed the peak of disease in EAN mice. Ginkgolides also down-regulated the proportions of T helper (Th) 17 cells in EAN spleens. Furthermore, we also found that administration of ginkgolides significantly decreased the levels of interferon (IFN)-γ and interleukin-12 (IL)-12 in GBS patients. Our results suggested that ginkgolides ameliorated the clinical score of EAN through down-regulating the proportions of Th 17 cells. Ginkgolides also suppressed inflammation response by decreasing pro-inflammatory cytokines IFN-γ and IL-12, suggesting ginkgolides had potential therapeutic effects on GBS patients and EAN in the future.

Sections du résumé

BACKGROUND BACKGROUND
Guillain-Barré syndrome (GBS) is an acquired immune-mediated inflammatory peripheral neuropathy. The immune regulation of ginkgolides have been revealed in recent years. We herein investigate the potential therapeutic effects of ginkgolides both on GBS and its animal model, experimental autoimmune neuritis (EAN).
METHODS METHODS
EAN in C57BL/6 mice induced by subcutaneous injection with peripheral nerve myelin P0 protein peptide 180-199 (P0 peptide) were treated with ginkgolides at three different doses. GBS patients were randomly divided into two groups, the experimental group and the control group. The experimental group were treated with ginkgolides as soon as diagnosed.
RESULTS RESULTS
Our data indicated that ginkgolides administration daily ameliorated the score of EAN and delayed the peak of disease in EAN mice. Ginkgolides also down-regulated the proportions of T helper (Th) 17 cells in EAN spleens. Furthermore, we also found that administration of ginkgolides significantly decreased the levels of interferon (IFN)-γ and interleukin-12 (IL)-12 in GBS patients.
CONCLUSIONS CONCLUSIONS
Our results suggested that ginkgolides ameliorated the clinical score of EAN through down-regulating the proportions of Th 17 cells. Ginkgolides also suppressed inflammation response by decreasing pro-inflammatory cytokines IFN-γ and IL-12, suggesting ginkgolides had potential therapeutic effects on GBS patients and EAN in the future.

Identifiants

pubmed: 33863532
pii: S0967-5868(21)00089-8
doi: 10.1016/j.jocn.2021.02.016
pii:
doi:

Substances chimiques

Cytokines 0
Ginkgolides 0
Myelin P0 Protein 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

44-49

Informations de copyright

Copyright © 2021 Elsevier Ltd. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

Chunrong Li (C)

Neuroscience Center, Department of Neurology, The First Hospital of Jilin University, Jilin University, Changchun, China.

Shan Liu (S)

Neuroscience Center, Department of Neurology, The First Hospital of Jilin University, Jilin University, Changchun, China.

Qiaolifan Aerqin (Q)

Neuroscience Center, Department of Neurology, The First Hospital of Jilin University, Jilin University, Changchun, China.

Donghui Shen (D)

Neuroscience Center, Department of Neurology, The First Hospital of Jilin University, Jilin University, Changchun, China.

Xiujuan Wu (X)

Neuroscience Center, Department of Neurology, The First Hospital of Jilin University, Jilin University, Changchun, China.

Kangding Liu (K)

Neuroscience Center, Department of Neurology, The First Hospital of Jilin University, Jilin University, Changchun, China. Electronic address: liukd@jlu.edu.cn.

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Classifications MeSH