Abstract: Eupatilin (5,7-dihydroxy-3′,4′,6-trimethoxyflavone), an extract from Artemisia asiatica Nakai, is a flavonoid of pharmacologically active ingredients. Eupatilin is known to possess anti-cancer, anti-inflammatory, and anti-oxidative activity. Recently, eupatilin has been reported to be effective in producing gastric mucosal as an anti-gastritis agents. However, the mechanism of protective action is still unknown. We studied cytoprotective actions of eupatilin on H2O2-induced cell death and its possible mechanisms of action in human gastric (AGS) cells. Eupatilin dose-dependently inhibited H2O2-induced apoptosis as indicated by co-staining with Annexin V and propidium iodide. Hydrogen peroxide provoked phosphorylation of extracellular regulated kinase (ERK) and c-Jun NH2-terminal kinase (JNK), and activation of nuclear factor-κB (NF-κB). On the contrary, eupatilin decreased H2O2-induced activation of ERK, JNK and NF-κB. In addition, treatment of specific inhibitors for ERK, JNK, and NF-κB attenuated H2O2-induced apoptosis. Co-treatment of inhibitors and eupatilin was more effective in decreasing H2O2-induced apoptosis. Taken together, we suggest that eupatilin inhibits H2O2-induced apoptosis through the inhibition ERK, JNK, and NF-κB. [Copyright 2008 Elsevier] Copyright of Food & Chemical Toxicology is the property of Pergamon Press - An Imprint of Elsevier Science and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts)