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Intestinal trefoil factor (ITE also named as trefoil factor 3, TFF3) is a member of the TFF-domain peptide family,which plays an essential role in regulating cell survival, cell migration and maintainsmucosal epithelial integrity in gastrointestinal tract.However, the underlying mechanisms and associated molecules remain unclear.The aim of this study was to explore the protective effects of ITF on gastric mucosal epithelium injury and its possible molecular mechanism.In the present study, we show that ITF could promote proliferation and migration of GES-1 cells via a mechanism that involves the PI3K/Akt signaling pathway.Western blot results indicated thatITF induced a dose-and time-dependent increase in Akt signaling pathway.ITF also plays an essential role in restitution of GES-1 cells damage induced by LPS (Lipopolysaccharide).LPS induced GES-1 cells apoptosis,decreased cell viability significantly (P <0.01) and led epithelial tight junction damage which is attenuated via ITF treated.The protective effect of ITF on the integrity of GES-1 was abrogated by inhibition of the PI3K/Akt pathway.Taken together, our results demonstrate that ITF promotes proliferation and migration of gastric mucosal epithelial cells and preservesgastric mucosal epithelialintegrityafter damageis mediated by activation of PI3K/Akt signaling pathway.This study suggested that PI3K/Akt pathway could act as a key intracellular pathway in the gastric mucosal epithelium that may serve as a therapeutic target to preserve epithelial integrity during injury.