{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,7]],"date-time":"2026-09-07T20:30:50Z","timestamp":1788813050247,"version":"build-2803163510"},"reference-count":38,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2023,12,6]],"date-time":"2023-12-06T00:00:00Z","timestamp":1701820800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["analyticalsciencejournals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Applied Toxicology"],"published-print":{"date-parts":[[2024,4]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:label\/><jats:p><jats:italic>Helicobacter pylori<\/jats:italic> (HP) infection is the main cause of most cases of gastritis. Quercetin has been shown to have anti\u2010inflammatory, anti\u2010bacterial, and antiviral activities and has been demonstrated to be involved in HP\u2010induced gastric mucosa injury. Moreover, the secretory protein lipocalin\u20102 (LCN2) was elevated in HP\u2010infected gastric mucosa. Thus, this work aimed to study the interaction between quercetin and LCN2 in HP\u2010triggered gastric injury during gastritis. Human gastric epithelial cell line GES\u20101 cells were exposed to HP for functional experiments. Cell viability, apoptosis, and inflammation were evaluated by cell counting kit\u20108, flow cytometry, and enzyme\u2010linked immunosorbent assay, respectively. Levels of genes and proteins were tested using quantitative reverse transcription polymerase chain reaction and western blotting analyses. The interaction between LCN2 and specificity protein 1 (SP1) was validated using chromatin immunoprecipitation assay and dual\u2010luciferase reporter assay. Thereafter, we found quercetin treatment suppressed HP\u2010induced GES\u20101 cell apoptotic and inflammatory injury and macrophage M1 polarization. LCN2 was highly expressed in HP\u2010infected gastritis patients and HP\u2010infected GES\u20101 cells, while quercetin reduced LCN2 expression in HP\u2010infected GES\u20101 cells; moreover, LCN2 knockdown reversed HP\u2010induced GES\u20101 cell injury and macrophage M1 polarization, and forced expression of LCN2 abolished the protective effects of quercetin on GES\u20101 cells under HP infection. Mechanistically, SP1 bound to LCN2 promoter and promoted its transcription. Also, SP1 overexpression counteracted the functions of quercetin on HP\u2010stimulated GES\u20101 cells. In all, quercetin ameliorated HP\u2010induced gastric epithelial cell apoptotic and inflammatory injuries, and macrophage M1 polarization via the SP1\/LCN2 axis.<\/jats:p><\/jats:sec>","DOI":"10.1002\/jat.4566","type":"journal-article","created":{"date-parts":[[2023,12,7]],"date-time":"2023-12-07T06:33:38Z","timestamp":1701930818000},"page":"641-650","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":12,"title":["Quercetin ameliorates <scp><i>Helicobacter\u2009pylori<\/i><\/scp>\u2010induced gastric epithelial cell injury by regulating specificity protein 1\/lipocalin 2 axis in gastritis"],"prefix":"10.1002","volume":"44","author":[{"ORCID":"https:\/\/orcid.org\/0009-0006-6351-8458","authenticated-orcid":false,"given":"Ziwei","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Gastroenterology, The First Affiliated Hospital Zhejiang University School of Medicine  Hangzhou 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