{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["9"],"submitter":["Colucci R"],"pubmed_abstract":["Non-steroidal anti-inflammatory drugs (NSAIDs) can damage the small intestine, mainly through an involvement of enteric bacteria. This study examined the pathophysiology of NSAID-associated intestinal lesions in a rat model of diclofenac-enteropathy and evaluated the effect of rifaximin on small bowel damage. Enteropathy was induced in 40-week old male rats by intragastric diclofenac (4 mg/kg BID, 14 days). Rifaximin (delayed release formulation) was administered (50 mg/kg BID) 1 h before the NSAID. At the end of treatments, parameters dealing with ileal damage, inflammation, barrier integrity, microbiota composition, and TLR-NF-κB-inflammasome pathway were evaluated. In addition, the modulating effect of rifaximin on NLRP3 inflammasome was tested in an <i>in vitro</i> cell system. Diclofe"],"journal":["Frontiers in pharmacology"],"pagination":["1340"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6281992"],"repository":["biostudies-literature"],"pubmed_title":["Pathophysiology of NSAID-Associated Intestinal Lesions in the Rat: Luminal Bacteria and Mucosal Inflammation as Targets for Prevention."],"pmcid":["PMC6281992"],"pubmed_authors":["Scarpignato C","Gentile D","Fulceri F","Tirotta E","Fornai M","Benvenuti L","Colucci R","Natale G","Pellegrini C","Antonioli L","Palazon-Riquelme P","Renzulli C","Ghelardi E","Piccoli E","Blandizzi C","Lopez-Castejon G"],"additional_accession":[]},"is_claimable":false,"name":"Pathophysiology of NSAID-Associated Intestinal Lesions in the Rat: Luminal Bacteria and Mucosal Inflammation as Targets for Prevention.","description":"Non-steroidal anti-inflammatory drugs (NSAIDs) can damage the small intestine, mainly through an involvement of enteric bacteria. This study examined the pathophysiology of NSAID-associated intestinal lesions in a rat model of diclofenac-enteropathy and evaluated the effect of rifaximin on small bowel damage. Enteropathy was induced in 40-week old male rats by intragastric diclofenac (4 mg/kg BID, 14 days). Rifaximin (delayed release formulation) was administered (50 mg/kg BID) 1 h before the NSAID. At the end of treatments, parameters dealing with ileal damage, inflammation, barrier integrity, microbiota composition, and TLR-NF-κB-inflammasome pathway were evaluated. In addition, the modulating effect of rifaximin on NLRP3 inflammasome was tested in an <i>in vitro</i> cell system. Diclofe","dates":{"release":"2018-01-01T00:00:00Z","publication":"2018","modification":"2026-05-06T03:09:29.697Z","creation":"2019-03-27T00:12:16Z"},"accession":"S-EPMC6281992","cross_references":{"pubmed":["30555323"],"doi":["10.3389/fphar.2018.01340"]}}