Melatonin suppresses inflammation and blood‒brain barrier disruption in rats with vascular dementia possibly by activating the SIRT1/PGC-1α/PPARγ signaling pathway.


Journal

Inflammopharmacology
ISSN: 1568-5608
Titre abrégé: Inflammopharmacology
Pays: Switzerland
ID NLM: 9112626

Informations de publication

Date de publication:
Jun 2023
Historique:
received: 01 12 2022
accepted: 25 02 2023
medline: 1 6 2023
pubmed: 6 4 2023
entrez: 5 4 2023
Statut: ppublish

Résumé

Chronic cerebral hypoxia (CCH) is caused by a reduction in cerebral blood flow, and cognitive impairment has been the predominant feature that occurs after CCH. Recent reports have revealed that melatonin is proficient in neurodegenerative diseases. However, the molecular mechanism by which melatonin affects CCH remains uncertain. In this study, we aimed to explore the role and underlying mechanism of melatonin in inflammation and blood‒brain barrier conditions in rats with CCH. Male Wistar rats were subjected to permanent bilateral common carotid artery occlusion (BCCAO) to establish the VAD model. Rats were randomly divided into four groups: Sham, BCCAO, BCCAO treated with melatonin (10 mg/kg), and BCCAO treated with resveratrol (20 mg/kg). All drugs were administered once daily for 4 weeks. Our results showed that melatonin attenuated cognitive impairment, as demonstrated by the Morris water maze tests. Furthermore, melatonin reduced the activation of inflammation by attenuating the phosphorylated nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor alpha (pIκBα), causing the suppression of proteins related to inflammation and inflammasome formation. Moreover, immunohistochemistry revealed that melatonin reduced glial cell activation and proliferation, which were accompanied by Western blotting results. Additionally, melatonin also promoted the expression of sirtuin-1 (SIRT1), peroxisome proliferator-activated receptor-gamma coactivator 1-alpha (PGC-1α), and peroxisome proliferator-activated receptor-gamma (PPARγ), causing attenuated blood‒brain barrier (BBB) disruption by increasing tight junction proteins. Taken together, our results prove that melatonin treatment modulated inflammation and BBB disruption and improved cognitive function in VaD rats, partly by activating the SIRT1/PGC-1α/PPARγ signaling pathway.

Identifiants

pubmed: 37017851
doi: 10.1007/s10787-023-01181-5
pii: 10.1007/s10787-023-01181-5
doi:

Substances chimiques

Melatonin JL5DK93RCL
Sirtuin 1 EC 3.5.1.-
PPAR gamma 0
Sirt1 protein, rat EC 3.5.1.-

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1481-1493

Subventions

Organisme : Thailand Science Research and Innovation (TSRI)
ID : 64/004
Organisme : Thailand and the Development and Promotion of Science and Technology Talents Project Royal Government of Thailand scholarship
ID : 572109

Informations de copyright

© 2023. The Author(s), under exclusive licence to Springer Nature Switzerland AG.

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Auteurs

Phakkawat Thangwong (P)

Department of Physiology, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand.
Graduate School, Chiang Mai University, Chiang Mai, 50200, Thailand.

Pranglada Jearjaroen (P)

Department of Physiology, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand.

Chainarong Tocharus (C)

Department of Anatomy, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand.

Piyarat Govitrapong (P)

Chulabhorn Graduate Institute, Kamphaeng Phet 6 Road, Lak Si, Bangkok, 10210, Thailand.

Jiraporn Tocharus (J)

Department of Physiology, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand. jiraporn.tocharus@cmu.ac.th.
Functional Food Research Center for Well-being, Chiang Mai University, Chiang Mai, 50200, Thailand. jiraporn.tocharus@cmu.ac.th.

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