{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T12:15:01Z","timestamp":1790079301935,"version":"4.0.1"},"reference-count":55,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2026,6,23]],"date-time":"2026-06-23T00:00:00Z","timestamp":1782172800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,6,23]],"date-time":"2026-06-23T00:00:00Z","timestamp":1782172800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Biochem &amp;amp; Molecular Tox"],"published-print":{"date-parts":[[2026,7]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    <jats:italic>Helicobacter pylori<\/jats:italic>\n                    infection is a major risk factor for gastric cancer (GC), but the molecular mechanisms remain incompletely understood. This exploratory in vitro study investigated whether treatment with the flavonoid morin correlates with altered expression of MAPK\/Nrf2\/STAT\u20103 pathway proteins in\n                    <jats:italic>H. pylori<\/jats:italic>\n                    \u2010infected human gastric epithelial cells (GES\u20101). GES\u20101 cells were infected with\n                    <jats:italic>H. pylori<\/jats:italic>\n                    (ATCC 49503, MOI 100:1) and treated with 40\u2009\u00b5M morin for 24\u2009h. Outcomes included cell viability (MTT assay), ROS production (DCFH\u2010DA), oxidative DNA damage (comet assay), glutathione and malondialdehyde levels (biochemical assays), protein expression (Western blot), and gene expression (RT\u2010PCR). Molecular docking predicted binding affinity between morin and pathway proteins. This study used\n                    <jats:italic>n<\/jats:italic>\n                    \u2009=\u20093 biological replicates per group and a lenient false discovery rate threshold (\n                    <jats:italic>Q<\/jats:italic>\n                    \u2009=\u20090.25) appropriate for hypothesis generation; findings require independent replication.\n                  <\/jats:p>\n                  <jats:p>\n                    In this exploratory study, morin treatment (40\u2009\u00b5M) was associated with:\n                    <jats:list list-type=\"bullet\">\n                      <jats:list-item>\n                        <jats:p>\n                          Higher MTT\u2010detectable viability in\n                          <jats:italic>H. pylori<\/jats:italic>\n                          \u2010infected cultures compared to infected untreated controls (85% vs. 45%;\n                          <jats:italic>q<\/jats:italic>\n                          \u2009=\u20090.042)\n                        <\/jats:p>\n                      <\/jats:list-item>\n                      <jats:list-item>\n                        <jats:p>\n                          Lower intracellular ROS levels (\n                          <jats:italic>q<\/jats:italic>\n                          \u2009=\u20090.021) and reduced oxidative DNA damage (\n                          <jats:italic>q<\/jats:italic>\n                          \u2009=\u20090.018) compared to infected untreated controls\n                        <\/jats:p>\n                      <\/jats:list-item>\n                      <jats:list-item>\n                        <jats:p>Higher GSH and lower MDA levels compared to infected untreated controls<\/jats:p>\n                      <\/jats:list-item>\n                      <jats:list-item>\n                        <jats:p>Lower phosphorylation levels of MAPK family members (ERK, JNK, p38), PI3K\/AKT, and STAT3\/EGFR proteins compared to infected untreated controls<\/jats:p>\n                      <\/jats:list-item>\n                      <jats:list-item>\n                        <jats:p>Higher total Nrf2 protein expression and upregulation of HMOX1 and NQO1 mRNA compared to infected untreated controls<\/jats:p>\n                      <\/jats:list-item>\n                    <\/jats:list>\n                  <\/jats:p>\n                  <jats:p>\n                    Molecular docking predicted binding between morin and MAPK, STAT3, and NRF2 pathway proteins, but these computational findings require experimental validation. These correlative findings are consistent with the hypothesis that morin treatment engages MAPK\/Nrf2\/STAT\u20103 pathways in\n                    <jats:italic>H. pylori<\/jats:italic>\n                    \u2010infected GES\u20101 cells. However, this study does not establish causality, Nrf2 activation (nuclear translocation not demonstrated), or therapeutic efficacy (no positive controls). The observed associations should be interpreted as hypothesis\u2010generating and require independent replication, mechanistic validation (including Nrf2 loss\u2010of\u2010function experiments), and comparative studies with standard agents before any translational inference. Under the specific in vitro conditions tested (GES\u20101 cells, H. pylori ATCC 49503, 40\u2009\u00b5M morin, 24\u2010h exposure,\n                    <jats:italic>n<\/jats:italic>\n                    \u2009=\u20093 biological replicates), morin treatment was associated with lower ROS levels, reduced MAPK\/STAT3 phosphorylation, and higher Nrf2 protein expression compared to infected untreated controls. These correlative findings are hypothesis\u2010generating and do not establish therapeutic potential, safety, efficacy, or clinical relevance. Independent replication, comprehensive toxicological characterization (including normal cell lines and in vivo models), direct comparison with standard agents (clarithromycin, sulforaphane), and mechanistic validation (including Nrf2 loss\u2010of\u2010function experiments) are required before any consideration of morin for further development. This study provides no evidence to support morin as a therapeutic, adjuvant, or alternative agent.\n                  <\/jats:p>","DOI":"10.1002\/jbt.70935","type":"journal-article","created":{"date-parts":[[2026,6,23]],"date-time":"2026-06-23T07:01:19Z","timestamp":1782198079000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Correlates of MAPK\/Nrf2\/STAT\u20103 Pathway Protein Expression With Morin Treatment in\n                    <i>Helicobacter pylori<\/i>\n                    \u2010Infected Gastric Epithelial Cells\u20101 Cells: An Exploratory In Vitro Study"],"prefix":"10.1002","volume":"40","author":[{"ORCID":"https:\/\/orcid.org\/0009-0006-2414-4123","authenticated-orcid":false,"given":"Yanping","family":"Zhang","sequence":"first","affiliation":[{"name":"Department of Gastroenterology, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Third Hospital of Shanxi Medical University Tongji Shanxi Hospital Taiyuan China"},{"name":"Faculty of Graduate Studies Shanxi Medical University Taiyuan Shanxi China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,6,23]]},"reference":[{"key":"e_1_2_13_2_1","doi-asserted-by":"publisher","DOI":"10.3322\/caac.21660"},{"key":"e_1_2_13_3_1","doi-asserted-by":"publisher","DOI":"10.1007\/s10120-017-0716-7"},{"key":"e_1_2_13_4_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.scitotenv.2021.148546"},{"key":"e_1_2_13_5_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.chom.2014.02.008"},{"issue":"1","key":"e_1_2_13_6_1","first-page":"936","article-title":"88. 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