Boric Acid Alleviates Gastric Ulcer by Regulating Oxidative Stress and Inflammation-Related Multiple Signaling Pathways.

AMPK Gastric ulcer Homocysteine IL-6/JAK2/STAT3 pathway Inflammation Sema3A/PlexinA1

Journal

Biological trace element research
ISSN: 1559-0720
Titre abrégé: Biol Trace Elem Res
Pays: United States
ID NLM: 7911509

Informations de publication

Date de publication:
May 2024
Historique:
received: 03 08 2023
accepted: 16 08 2023
pubmed: 22 8 2023
medline: 22 8 2023
entrez: 22 8 2023
Statut: ppublish

Résumé

Oxidative stress and inflammation have pivotal roles in gastric ulcer development caused by alcohol consumption. Trace element boric acid taken into the human and animal body from dietary sources displays strong antioxidant and anti-inflammatory functions. However, the mechanisms underlying these actions of boric acid remain unclear, and its effectiveness in preventing gastric lesions is unknown. Therefore, the present study was undertaken to evaluate the protective effects of boric acid in alcohol-induced gastric ulcer and elucidate its potential mechanisms. Gastric ulcer was induced by 75% oral ethanol administration in rats, and the effectiveness of prophylactic boric acid treatment at 100 mg/kg concentration was assessed by histopathological examination, ELISA assay and qRT-PCR. Gross macroscopic and histopathological evaluations revealed that boric acid alleviated gastric mucosal lesions. Boric acid decreased reactive oxygen species (ROS) and malondialdehyde (MDA) concentration and the overall oxidation state of the body while improving antioxidant status. It reduced the concentration of tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6). The mRNA expression of JAK2 and STAT3 was decreased while the expression of AMPK was increased with boric acid pretreatment. Moreover, Sema3A and PlexinA1 levels were elevated upon boric acid pretreatment, and homocysteine levels were reduced. Our results demonstrated that boric acid protects gastric mucosa from ethanol-induced damage by regulating oxidative and inflammatory responses. In addition, our findings suggested that the gastroprotective activity of boric acid could be attributed to its regulatory function in the IL-6/JAK2/STAT3 signaling modulated by AMPK and that Sema3A/PlxnA1 axis and homocysteine are potentially involved in this process.

Identifiants

pubmed: 37606879
doi: 10.1007/s12011-023-03817-7
pii: 10.1007/s12011-023-03817-7
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

2124-2132

Subventions

Organisme : Kütahya Health Sciences University
ID : FBA-2021-88

Informations de copyright

© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.

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Auteurs

Ayşe Çakır Gündoğdu (AÇ)

Department of Histology and Embryology, Faculty of Medicine, Kütahya Health Sciences University, Kütahya, Türkiye.

Cansu Özbayer (C)

Department of Medical Biology, Faculty of Medicine, Kütahya Health Sciences University, Kütahya, Türkiye.

Fatih Kar (F)

Department of Medical Biochemistry, Faculty of Medicine, Kütahya Health Sciences University, Evliya Çelebi Campus, 10th km of the Tavşanlı Road, 43100, Kütahya, Türkiye. fatih.kar@ksbu.edu.tr.

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