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Nesfatin-1 alleviates gastric damage via direct antioxidant mechanisms

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dc.contributor.authorYEGEN, BERRAK
dc.contributor.authorsKolgazi, Meltem; Cantali-Ozturk, Cigdem; Deniz, Rabia; Ozdemir-Kumral, Zarife Nigar; Yuksel, Meral; Sirvanci, Serap; Yegen, Berrak C.
dc.date.accessioned2022-03-13T12:48:45Z
dc.date.available2022-03-13T12:48:45Z
dc.date.issued2015
dc.description.abstractBackground: Indomethacin is a nonsteroidal anti-inflammatory drug, which is known to produce serious side effects, causing ulcerative lesions. Nesfatin-1, a newly identified anorexigenic peptide, was recently shown to have neuroprotective effects. The aim of the study was to investigate the anti-inflammatory effects of nesfatin-1 on indomethacin-induced gastric ulcer. Materials and methods: After a 24-h starvation period, ulcer was induced in Sprague-Dawley rats by subcutaneous administration of indomethacin (25 mg/kg), whereas control group received vehicle. Fifteen minutes after ulcer induction, rats were treated with either saline or nesfatin-1 (0.1, 0.3, or 1 mu g/kg, intraperitoneally). At the fourth hour, all rats were decapitated and their trunk blood was collected for tumor necrosis factor (TNF)-alpha and interleukin (IL)-6 measurements. Stomach samples were examined microscopically and analyzed for myeloperoxidase (MPO) activity, malondialdehyde (MDA), glutathione (GSH), luminol-, and lucigenin-enhanced chemiluminescence (CL) levels. Results: Ulcer induction increased serum TNF-alpha; and IL-6 levels, gastric CL and MDA levels and MPO activity but decreased gastric GSH content (P < 0.05-0.001). On the other hand, 0.1 mu g/kg dose of nesfatin-1 reduced microscopic and macroscopic damage scores, decreased MPO activity and MDA levels, CL and IL-6 levels, whereas gastric GSH was replenished (P < 0.01). However, indomethacin-induced increase in TNF-alpha level was abolished at only 1 mu g/kg dose of nesfatin-1 (P < 0.01). Conclusions: Nesfatin-1 alleviated indomethacin-induced gastric injury, suggesting that the anti-inflammatory and gastroprotective effects of nesfatin-1 on oxidative gastric damage could be implemented by supporting the balance in oxidant and antioxidant systems while inhibiting the generation of pro-inflammatory mediators. (C) 2015 Elsevier Inc. All rights reserved.
dc.identifier.doi10.1016/j.jss.2014.06.057
dc.identifier.eissn1095-8673
dc.identifier.issn0022-4804
dc.identifier.pubmed25082746
dc.identifier.urihttps://hdl.handle.net/11424/238238
dc.identifier.wosWOS:000346241300014
dc.language.isoeng
dc.publisherACADEMIC PRESS INC ELSEVIER SCIENCE
dc.relation.ispartofJOURNAL OF SURGICAL RESEARCH
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectUlcer
dc.subjectIndomethacin
dc.subjectNesfatin-1
dc.subjectGastric damage
dc.subjectAntioxidant
dc.subjectTUMOR-NECROSIS-FACTOR
dc.subjectFREE-RADICALS
dc.subjectNITRIC-OXIDE
dc.subjectINDOMETHACIN
dc.subjectINJURY
dc.subjectRAT
dc.subjectINFILTRATION
dc.subjectPATHOGENESIS
dc.subjectINFLAMMATION
dc.subjectGLUTATHIONE
dc.titleNesfatin-1 alleviates gastric damage via direct antioxidant mechanisms
dc.typearticle
dspace.entity.typePublication
local.avesis.idd3e53426-0b0d-4c68-9c98-4a8946bbbc01
local.import.packageSS17
local.indexed.atWOS
local.indexed.atSCOPUS
local.indexed.atPUBMED
local.journal.numberofpages8
oaire.citation.endPage118
oaire.citation.issue1
oaire.citation.startPage111
oaire.citation.titleJOURNAL OF SURGICAL RESEARCH
oaire.citation.volume193
relation.isAuthorOfPublicatione4eaf9ac-f8dc-4e2b-b940-895cc906790d
relation.isAuthorOfPublication.latestForDiscoverye4eaf9ac-f8dc-4e2b-b940-895cc906790d

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