Syringic acid guards against indomethacin-induced gastric ulcer by alleviating inflammation, oxidative stress and apoptosis

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The purpose of this study was to evaluate the effects of syringic acid, an anti-oxidant, on indomethacin induced gastric ulcers in rats. Experimental groups were control, ulcer, ulcer treated with 20 mg/kg esomeprazole (a proton pump inhibitor that reduces acid secretion), and ulcer treated with 100 mg/kg syringic acid. Rats were pretreated with esomeprazole or syringic acid two weeks before ulcer induction. Our histopathological observations showed that either syringic acid or esomeprazole attenuated the severity of gastric mucosal damage. Moreover, syringic acid and esomeprazole pretreatments alleviated indomethacin-induced damage by regulating oxidative stress, inflammatory response, the level of transforming growth factor-β (TGF-β), expressions of COX and prostaglandin E2, cell proliferation, apoptosis and regulation of the NF-κB signaling pathway. We conclude that either esomeprazole or syringic acid administration protected the gastric mucosa from harmful effects of indomethacin. Syringic acid might, therefore be a potential therapeutic agent for preventing and treating indomethacin-induced gastric damage. © 2024 The Biological Stain Commission.

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AlanDeğerDil
dc.contributor.authorFerah Okkay, Irmak
dc.contributor.authorOkkay, Ufuk
dc.contributor.authorCicek, Betul
dc.contributor.authorKaratas, Ozhan
dc.contributor.authorYilmaz, Aysegul
dc.contributor.authorYesilyurt, Fatma
dc.contributor.authorHacimuftuoglu, Ahmet
dc.date.accessioned2026-10-18T20:26:53.922041133Z
dc.date.available2026-10-18T20:26:53.922041133Z
dc.date.issued2024
dc.description.abstractThe purpose of this study was to evaluate the effects of syringic acid, an anti-oxidant, on indomethacin induced gastric ulcers in rats. Experimental groups were control, ulcer, ulcer treated with 20 mg/kg esomeprazole (a proton pump inhibitor that reduces acid secretion), and ulcer treated with 100 mg/kg syringic acid. Rats were pretreated with esomeprazole or syringic acid two weeks before ulcer induction. Our histopathological observations showed that either syringic acid or esomeprazole attenuated the severity of gastric mucosal damage. Moreover, syringic acid and esomeprazole pretreatments alleviated indomethacin-induced damage by regulating oxidative stress, inflammatory response, the level of transforming growth factor-β (TGF-β), expressions of COX and prostaglandin E2, cell proliferation, apoptosis and regulation of the NF-κB signaling pathway. We conclude that either esomeprazole or syringic acid administration protected the gastric mucosa from harmful effects of indomethacin. Syringic acid might, therefore be a potential therapeutic agent for preventing and treating indomethacin-induced gastric damage. © 2024 The Biological Stain Commission.
dc.identifier.doi10.1080/10520295.2024.2344477
dc.identifier.eissn1473-7760
dc.identifier.endpage156
dc.identifier.issn1052-0295
dc.identifier.issue3
dc.identifier.pmid38644776
dc.identifier.scopus2-s2.0-85191183698
dc.identifier.startpage147
dc.identifier.urihttps://rdlopen.rawdatalibrary.net/r/ebyu/11919
dc.identifier.volume99
dc.identifier.wosWOS:001207014300001
dc.language.isoen
dc.publisherTaylor and Francis Ltd.
dc.relation.ispartofBiotechnic and Histochemistry
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectGastric ulcer
dc.subjectindomethacin
dc.subjectNF-κB
dc.subjectoxidative stress
dc.subjectsyringic acid
dc.subjectAnimals
dc.subjectApoptosis
dc.subjectEsomeprazole
dc.subjectGallic Acid
dc.subjectGastric Mucosa
dc.subjectInflammation
dc.subjectMale
dc.subjectRats
dc.subjectRats, Sprague-Dawley
dc.subjectStomach Ulcer
dc.subjectindometacin
dc.subjectanimal
dc.subjectdrug effect
dc.subjectpathology
dc.subjectrat
dc.subjectSprague Dawley rat
dc.subjectstomach mucosa
dc.titleSyringic acid guards against indomethacin-induced gastric ulcer by alleviating inflammation, oxidative stress and apoptosis
dc.typeArticle
dspace.entity.typePublication
rdl.citation.scopus13
rdl.citation.wos9
rdl.departmentDepartment of Physiology, Faculty of Medicine, Erzincan Binali Yildirim University, Erzincan, Turkey.
rdl.source.indexSCOPUS
rdl.source.indexWOS
rdl.source.indexPUBMED
rdl.wos.indexScience Citation Index Expanded (SCI-EXPANDED)