Insulin-like growth factor attenuates apoptosis and mucosal damage in hypoxia/reoxygenation-induced intestinal injury

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dc.contributor.authorOzen S.
dc.contributor.authorAkisu M.
dc.contributor.authorBaka M.
dc.contributor.authorYalaz M.
dc.contributor.authorSozmen E.Y.
dc.contributor.authorBerdeli A.
dc.contributor.authorKultursay N.
dc.date.accessioned2019-10-27T00:11:02Z
dc.date.available2019-10-27T00:11:02Z
dc.date.issued2005
dc.departmentEge Üniversitesien_US
dc.description.abstractObjective: Necrotizing enterocolitis (NEC) is a potentially lethal disease among premature infants. The aim of the present study was to investigate whether hypoxia-reoxygenation (H/R)-induced intestinal injury was due to increased apoptosis of the intestinal mucosa in young mice and whether pre-treatment of the animals with recombinant human insulin-like growth factor-I (IGF-I), a known anti-apoptotic factor, could protect the intestinal cells from H/R-induced apoptosis or intestinal injury. Study Design: Young mice were divided into three groups: group 1 mice (H/R) were hypoxia-reoxygenation; group 2 mice (H/R + IGF-I) were treated with recombinant human IGF-I by intraperitoneal injection (1 µg/g b.w. once daily) for 7 days, and group 3 mice served as control. Hypoxia was induced by placing young mice in a Plexiglas chamber consisting of 10% oxygen for 60 min. After hypoxia, the young mice were reoxygenated for 10 min with 100% oxygen. Intestinal generation of substances reactive to thiobarbituric acid (TBARS) and active caspase-3 were measured in H/R-induced intestinal injury. Results: Increased numbers of apoptotic cells (apoptotic index) across the villi in young mice subjected to H/R were observed with the TUNEL reaction whereas few apoptotic cells existed in the control animals. In addition, H/R-induced intestinal damage in the H/R + IGF-I group was greatly attenuated, with necrosis limited partially to the mucosa. Tissue-active caspase-3 levels in the H/R group were found to be significantly higher when compared with that of the H/R + IGF-I group of mice and control. However, TBARS concentrations in the intestine were similar in H/R groups when compared to the intestine of control animals. Conclusion: The present study suggests that both necrosis and apoptosis, via mechanisms occurring due to oxygen-derived free radicals and activation of caspase-3, play a role in the pathogenesis of H/R-induced bowel injury. We also show that IGF-I protect intestinal mucosa from necrosis and apoptosis from intestinal H/R injury. Copyright © 2005 S. Karger AG, Basel.en_US
dc.identifier.doi10.1159/000081897en_US
dc.identifier.endpage96en_US
dc.identifier.issn0006-3126
dc.identifier.issue2en_US
dc.identifier.pmid15528875en_US
dc.identifier.scopusqualityN/Aen_US
dc.identifier.startpage91en_US
dc.identifier.urihttps://doi.org/10.1159/000081897
dc.identifier.urihttps://hdl.handle.net/11454/22098
dc.identifier.volume87en_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.relation.ispartofBiology of the Neonateen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectApoptosisen_US
dc.subjectCaspase-3en_US
dc.subjectIGF-Ien_US
dc.subjectInsulin-like growth factor-Ien_US
dc.subjectNecrotizing enterocolitisen_US
dc.titleInsulin-like growth factor attenuates apoptosis and mucosal damage in hypoxia/reoxygenation-induced intestinal injuryen_US
dc.typeArticleen_US

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