Abstract: Abstract: Objective To explore the influence of galangin in the antitumor effect of apatinib in gastric cancer cells and the underlying mechanism. Methods Human gastric cancer cell line SGC-7901 was cultured in vitro, and the satisfactory concentration of galangin and apatinib against SGC-7901 cells were determined by MTT assay. Gastric cancer cells were assigned to four groups: blank control group, galangin group, apatinib group and galangin+ apatinib group. Cell proliferation was determined by MTT assay, cell apoptosis was determined by flow cytometry assay, the migration and invasion of SGC-7901 cells were detected by wound healing and Transwell assay, respectively. Meanwhile, the expressions of related proteins were measured by Western blot assay. Results Both galangin and apatinib could significantly inhibit the proliferation of SGC-7901 cells in a dose-dependent manner (P＜0.05). Compared with apatinib group there was an enhanced inhibitory effects on cell proliferation, migration and invasion in galangin+apatinib group (P＜0.05). There was a significant promoted apoptosis in the galangin + apatinib group compared with that of 20 mg/L apatinib group (P＜0.05). Western blot showed that the expression levels of Bax, p-Akt and p-p38 were increased, and the level of Bcl-2 protein was significantly decreased, in galangin + apatinib group comparison with those of 20 mg / L apatinib group (P＜0.05). Conclusion Galangin can enhance antitumor effects of apatinib on gastric cancer SGC-7901 cells by inhibiting PI3K/Akt and activating p38-MAPK signaling pathway.

Key words: Galangin, stomach neoplasms, Apatinib, anti-cancer, PI3K/Akt signaling pathway, p38-MAPK signaling pathway