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http://purl.uniprot.org/citations/32574671http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/32574671http://www.w3.org/2000/01/rdf-schema#comment"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."xsd:string
http://purl.uniprot.org/citations/32574671http://purl.org/dc/terms/identifier"doi:10.1016/j.ejphar.2020.173265"xsd:string
http://purl.uniprot.org/citations/32574671http://purl.uniprot.org/core/author"Pasalar P."xsd:string
http://purl.uniprot.org/citations/32574671http://purl.uniprot.org/core/author"Abdollahi A."xsd:string
http://purl.uniprot.org/citations/32574671http://purl.uniprot.org/core/author"Dehpour A.R."xsd:string
http://purl.uniprot.org/citations/32574671http://purl.uniprot.org/core/author"Gharishvandi F."xsd:string
http://purl.uniprot.org/citations/32574671http://purl.uniprot.org/core/author"Mohammad Jafari R."xsd:string
http://purl.uniprot.org/citations/32574671http://purl.uniprot.org/core/author"Shafaroodi H."xsd:string
http://purl.uniprot.org/citations/32574671http://purl.uniprot.org/core/date"2020"xsd:gYear
http://purl.uniprot.org/citations/32574671http://purl.uniprot.org/core/name"Eur J Pharmacol"xsd:string
http://purl.uniprot.org/citations/32574671http://purl.uniprot.org/core/pages"173265"xsd:string
http://purl.uniprot.org/citations/32574671http://purl.uniprot.org/core/title"Involvement of 5-HT1B/1D receptors in the inflammatory response and oxidative stress in intestinal ischemia/reperfusion in rats."xsd:string
http://purl.uniprot.org/citations/32574671http://purl.uniprot.org/core/volume"882"xsd:string
http://purl.uniprot.org/citations/32574671http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/32574671
http://purl.uniprot.org/citations/32574671http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/32574671
http://purl.uniprot.org/uniprot/#_A6I1P1-mappedCitation-32574671http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/32574671
http://purl.uniprot.org/uniprot/#_A6ITB2-mappedCitation-32574671http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/32574671
http://purl.uniprot.org/uniprot/#_P28564-mappedCitation-32574671http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/32574671
http://purl.uniprot.org/uniprot/#_P28565-mappedCitation-32574671http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/32574671
http://purl.uniprot.org/uniprot/A6ITB2http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/32574671
http://purl.uniprot.org/uniprot/P28565http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/32574671
http://purl.uniprot.org/uniprot/A6I1P1http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/32574671
http://purl.uniprot.org/uniprot/P28564http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/32574671