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We previously reported that an aqueous extract of <jats:italic>A. capillaris<\/jats:italic> (AEAC) inhibited gastric inflammation induced by HCl\/ethanol via reactive oxygen species scavenging and NF\u2010\u03baB downregulation. To date, the pharmacological potential of AEAC for promoting mucosal integrity has not been studied.<\/jats:p><\/jats:sec><jats:sec><jats:title>RESULTS<\/jats:title><jats:p>Here, we report that a single treatment with AEAC increased mucus production, and repeated administration of AEAC abolished HCl\/ethanol\u2010induced mucosal injury <jats:italic>in vivo<\/jats:italic>. Single\u2010 and multiple\u2010dose AEAC treatments measurably increased the expression of mucosal stabilizing factors <jats:italic>in vivo<\/jats:italic>, including mucin (MUC) 5\u2009AC, MUC6, and trefoil factor (TFF) 1 and TFF2 (but not TFF3). AEAC also induced mucosal stabilizing factors in both SNU\u2010601 cells and RGM cells through phosphorylation of extracellular signal\u2010regulated kinases.<\/jats:p><\/jats:sec><jats:sec><jats:title>CONCLUSION<\/jats:title><jats:p>Taken together, our results suggest that AEAC protects against HCl\/ethanol\u2010induced gastritis by upregulating MUCs and TFFs and stabilizing the mucosal epithelium. \u00a9 2021 Society of Chemical Industry.<\/jats:p><\/jats:sec>","DOI":"10.1002\/jsfa.11463","type":"journal-article","created":{"date-parts":[[2021,8,6]],"date-time":"2021-08-06T14:15:46Z","timestamp":1628259346000},"page":"1255-1262","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["An aqueous extract from <scp><i>Artemisia capillaris<\/i><\/scp> inhibits acute gastric injury through mucosal stabilization"],"prefix":"10.1002","volume":"102","author":[{"given":"Su 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