Abstract: OBJECTIVE: To investigate the roles of endoplasmic reticulum stress (ERS) in apigenin (API) -induced apoptosis in human gastric cancer SGC-7901 cells. METHODS：SGC-7901 cells were treated with API at 20，40 ，60 and 80 μmol/L and at 3 μg/ml tunicamycin (TM) for 48 h or at 60 μmol/L for up to 48 h. GRP78，GRP94 and C/EBP-homologous protein ( CHOP) were explored using Western blot. When the cells were treated with endoplasmic reticulum stress inhibitor 4-phenyl butyric acid (4-PBA )，apoptosis was assessed by DAPI staining and flow cytometry. RESULTS：The protein levels of GRP78 and GRP94 increased in API-treated cells in time and dose -dependent manner，but apigenin did not induce the expression of CHOP protein. Pretreatment with 4-PBA drastically increased API-induced apoptosis in SGC-7901 cells (P<0.01). CONCLUSION：ERS may exert protective effect on API-induced apoptosis in human gastric cancer SGC-7901 cells.

Key words: endoplasmic reticulum stress, apigenin, apoptosis