<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>9</volume><submitter>Colucci R</submitter><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 &lt;i>in vitro&lt;/i> cell system. Diclofe</pubmed_abstract><journal>Frontiers in pharmacology</journal><pagination>1340</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6281992</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Pathophysiology of NSAID-Associated Intestinal Lesions in the Rat: Luminal Bacteria and Mucosal Inflammation as Targets for Prevention.</pubmed_title><pmcid>PMC6281992</pmcid><pubmed_authors>Scarpignato C</pubmed_authors><pubmed_authors>Gentile D</pubmed_authors><pubmed_authors>Fulceri F</pubmed_authors><pubmed_authors>Tirotta E</pubmed_authors><pubmed_authors>Fornai M</pubmed_authors><pubmed_authors>Benvenuti L</pubmed_authors><pubmed_authors>Colucci R</pubmed_authors><pubmed_authors>Natale G</pubmed_authors><pubmed_authors>Pellegrini C</pubmed_authors><pubmed_authors>Antonioli L</pubmed_authors><pubmed_authors>Palazon-Riquelme P</pubmed_authors><pubmed_authors>Renzulli C</pubmed_authors><pubmed_authors>Ghelardi E</pubmed_authors><pubmed_authors>Piccoli E</pubmed_authors><pubmed_authors>Blandizzi C</pubmed_authors><pubmed_authors>Lopez-Castejon G</pubmed_authors></additional><is_claimable>false</is_claimable><name>Pathophysiology of NSAID-Associated Intestinal Lesions in the Rat: Luminal Bacteria and Mucosal Inflammation as Targets for Prevention.</name><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 &lt;i>in vitro&lt;/i> cell system. Diclofe</description><dates><release>2018-01-01T00:00:00Z</release><publication>2018</publication><modification>2026-05-06T03:09:29.697Z</modification><creation>2019-03-27T00:12:16Z</creation></dates><accession>S-EPMC6281992</accession><cross_references><pubmed>30555323</pubmed><doi>10.3389/fphar.2018.01340</doi></cross_references></HashMap>