Involvement of 5-HT1B/1D receptors in the inflammatory response and oxidative stress in intestinal ischemia/reperfusion in rats.


Journal

European journal of pharmacology
ISSN: 1879-0712
Titre abrégé: Eur J Pharmacol
Pays: Netherlands
ID NLM: 1254354

Informations de publication

Date de publication:
05 Sep 2020
Historique:
received: 26 02 2020
revised: 04 06 2020
accepted: 08 06 2020
pubmed: 24 6 2020
medline: 14 5 2021
entrez: 24 6 2020
Statut: ppublish

Résumé

Acute mesenteric ischemia (AMI) is caused by an abrupt cessation of blood flow to the small intestine. Reperfusion is the return of blood flow to the ischemic bowel. Intestinal ischemia/reperfusion (I/R) leads to the formation of reactive oxygen species, local inflammatory response, and may lead to the patient's death. Pre-treatment of the intestinal may reduce the high mortality associated with AMI. 5-Hydroxytryptamine 1B (5-HT1B) and 5-HT1D receptors have anti-inflammatory and neuroprotective effects in different experimental studies. We aimed to investigate the potential involvement of these receptors in intestinal I/R injury. Firstly, we assessed the expression and localization of 5-HT1B and 5-HT1D receptors in the enteric nervous system using an immunofluorescence-based method. Intestinal I/R in rats was induced by 30 min occlusion of superior mesenteric artery and reperfusion for 2 h. Rats were randomly divided in different control and I/R groups (n = 6) receiving either vehicle, sumatriptan (5-HT1B/1D receptors agonist; 0.1 mg/kg), GR127,935 (5-HT1B/1D receptors antagonist; 0.1 mg/kg) and combination of sumatriptan (0.1 mg/kg) + GR127,935 (0.1 mg/kg) before determination of biochemical and histological parameters. In the enteric nervous system, 5-HT1B and 5-HT1D receptors were expressed 17% and 11.5%, respectively. Pre-treatment with sumatriptan decreased 5-hydroxytryptamine (5HT) level by 53%, and significantly decreased calcitonin gene-related peptide (CGRP) levels, lipid pereoxidation, neutrophil infiltration, and level of pro-inflammatory markers in the serum. Histopathologic studies also showed a remarkable decrease in intestinal tissue injury. These findings suggest that sumatriptan may inhibit intestinal injury induced by I/R through modulating the inflammatory response by activation of 5-HT1B/1D receptors.

Identifiants

pubmed: 32574671
pii: S0014-2999(20)30357-5
doi: 10.1016/j.ejphar.2020.173265
pii:
doi:

Substances chimiques

Oxadiazoles 0
Piperazines 0
Receptor, Serotonin, 5-HT1B 0
Receptor, Serotonin, 5-HT1D 0
Serotonin 5-HT1 Receptor Agonists 0
Serotonin Antagonists 0
GR 127935 2LLH6CEB40
Serotonin 333DO1RDJY
Sumatriptan 8R78F6L9VO
Calcitonin Gene-Related Peptide JHB2QIZ69Z

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

173265

Informations de copyright

Copyright © 2020 Elsevier B.V. All rights reserved.

Auteurs

Fatemeh Gharishvandi (F)

Department of Clinical Biochemistry, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.

Alireza Abdollahi (A)

Department of Pathology, School of Medicine, Tehran University of Medical Sciences, Imam Hospital Complex, Tehran, Iran.

Hamed Shafaroodi (H)

Department of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran; Experimental Medicine Research Center, Tehran University of Medical Sciences, Tehran, Iran.

Razieh Mohammad Jafari (R)

Experimental Medicine Research Center, Tehran University of Medical Sciences, Tehran, Iran.

Parvin Pasalar (P)

Department of Clinical Biochemistry, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. Electronic address: pasalar@sina.tums.ac.ir.

Ahmad Reza Dehpour (AR)

Department of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran; Experimental Medicine Research Center, Tehran University of Medical Sciences, Tehran, Iran; Brain and Spinal Injury Repair Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Electronic address: dehpoura@sina.tums.ac.ir.

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Classifications MeSH