Objective:To evaluate the effects of the ethanol extract isolated from Weiqi Decoction(胃祺饮,WQD-EE)on AGS cell proliferation and apoptosis.Methods:By using high-performance liquid chromatography with ultraviolet detectors(HPLC-UV)assay and MTT method,the main compounds in WQD-EE and cell viability were detected.And cell cycle distributions were determined by flow cytometry with propidium iodine(PI)staining while apoptosis was detected by flow cytometry with annexin V/Pl double staining.Finally,caspase-3 activities were measured by calorimetric method and protein expression was determined by Western blotting.Results:HPLC analysis showed that naringin(35.92μg/mg),nobiletin(21.98μg/mg),neohesperidin(17.98μg/mg)and tangeretin(0.756μg/mg)may be the main compounds in WQD-EE.WQD-EE not only inhibited AGS and MCF7 cell proliferation in a dose-dependent manner,but also blocked cell cycle progression at G_2/M stage as well as inducing cell apoptosis at concentrations triggering significant inhibition of proliferation and cell cycle arrest in AGS cells.While at 0.5 mg/mL,WQD-EE significantly increased caspase-3 activity by 2.75 and 7.47 times at 24 h and 48 h,respectively.Moreover,WQD-EE in one hand reduced protein expressions of p53 and cyclin B1,and in other hand enhanced protein expressions of cytochrome c and Bax.Protein levels of Bcl-2,Fas L and Fas were not significantly affected by WQD-EE.Conclusions:WQD-EE inhibits AGS cell proliferation through G_2/M arrest due to down-regulation of cyclin Bi protein expression,and promotes apoptosis by caspase-3 and mitochondria-dependent pathways,but not by p53-dependent pathway. Objective: To evaluate the effects of the ethanol extract isolated from Weiqi Decoction (AGQ) on AGS cell proliferation and apoptosis. Methods: By using high-performance liquid chromatography with ultraviolet detectors (HPLC-UV) assay and MTT assay of the main compounds in WQD-EE and cell viability were detected. And cell cycle distributions were determined by flow cytometry with propidium iodine (PI) staining while apoptosis was detected by flow cytometry with annexin V / Pl double staining. Finaally, caspase- 3 activities were measured by calorimetric method and protein expression was determined by Western blotting. Results: HPLC analysis showed that naringin (35.92 μg / mg), nobiletin (21.98 μg / mg), neohesperidin (17.98 μg / mg) and tangeretin / mg) may be the main compounds in WQD-EE. WQD-EE not only inhibited AGS and MCF7 cell proliferation in a dose-dependent manner, but also blocked cell cycle progression at G_2 / M stage as well as inducing cell apoptosis at concentrations triggering signific Inhibition of proliferation and cell cycle arrest in AGS cells. Whenever at 0.5 mg / mL, WQD-EE significantly increased caspase-3 activity by 2.75 and 7.47 times at 24 h and 48 h, respectively. Moreover, WQD-EE in one hand reduced protein expressions of p53 and cyclin B1, and in other hand enhanced protein expressions of cytochrome c and Bax. Protein levels of Bcl-2, Fas L and Fas were not significantly affected by WQD-EE. Conclusions: WQD-EE inhibits AGS cell proliferation through G_2 / M arrest due to down-regulation of cyclin Bi protein expression, and promote apoptosis by caspase-3 and mitochondria-dependent pathways, but not by p53-dependent pathway.