{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,3]],"date-time":"2026-06-03T11:28:59Z","timestamp":1780486139341,"version":"3.54.1"},"reference-count":53,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2024,1,21]],"date-time":"2024-01-21T00:00:00Z","timestamp":1705795200000},"content-version":"vor","delay-in-days":20,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["analyticalsciencejournals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Cell Biochemistry &amp;amp; Function"],"published-print":{"date-parts":[[2024,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Gastric ulceration is a prevalent worldwide clinical presentation due to altered gastric defense mechanisms. Nonsteroidal anti\u2010inflammatory drugs are one of the common causes of gastric ulcers mediated by the release of inflammatory mediators. The study aimed to investigate the potential protective effect of soyasaponin I (soya) against diclofenac (DIC)\u2010induced gastric ulcer in rats and to highlight the underlying mechanisms. The experiment was conducted on 40 male Wistar albino rats, equally distributed into five groups: control, DIC\u2010induced ulcer (9\u2009mg\/kg\/d, orally, twice daily for 3 days), ulcer\/soya\u2010, ulcer\/ranitidine\u2010, and ulcer\/soya\/selective nuclear factor kappa B inhibitor (JSH\u201023)\u2010treated groups. The doses of soya, ranitidine, and JSH were 20, 25, and 5\u2009mg\/kg\/d, respectively, given orally. Gastric specimens were prepared for gene and histological study and for biochemical analysis of gastric prostaglandin E2 (PGE2), oxidative markers, and inflammatory cytokines. The gastric samples were formalin\u2010fixed, paraffin\u2010embedded, and subjected to hematoxylin and eosin (H&amp;E), PAS staining, and immunohistochemical assay for identification of nuclear factor kappa B (NF\u2010\u03baB), cyclooxygenase\u20102 (COX\u20102), and proliferation marker (Ki67) expressions. The findings revealed decreased gastric PGE2 and altered inflammatory and oxidative markers in the ulcer model group. The H&amp;E staining showed mucosal injury characterized by mucosal surface defects and inflammatory cell infiltrations. The polymerase chain reaction (PCR) and immunohistochemistry demonstrated an upregulation of NF\u2010\u03baB and COX\u20102 expression at gene\/protein levels; meanwhile, Ki67 downregulation. The soya\u2010treated group showed maintained biochemical, histological, and PCR findings comparable to the ranitidine\u2010treated group. The JSH\u201023\u2010treated group still showed partial gastric protection with biochemical and immunohistochemical changes. Soyasaponin I ameliorated DIC\u2010induced gastric ulcers by targeting the COX\u20102 activity through modulation of NF\u2010\u03baB signaling.<\/jats:p>","DOI":"10.1002\/cbf.3927","type":"journal-article","created":{"date-parts":[[2024,1,22]],"date-time":"2024-01-22T00:16:38Z","timestamp":1705882598000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":12,"title":["Targeting NF\u2010\u03baB\/COX\u20102 signaling by soyasaponin I alleviates diclofenac\u2010induced gastric ulceration in male albino rats"],"prefix":"10.1002","volume":"42","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-7911-0795","authenticated-orcid":false,"given":"Ahmed A.","family":"Morsi","sequence":"first","affiliation":[{"name":"Department of Histology and Cell Biology, Faculty of Medicine Fayoum University Fayoum Egypt"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lamiaa 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