AIM: To investigate the synergistic effect of oxymatrine(OM) and angiogenesis inhibitor NM-3 on modulatingapoptosis in human gastric cancer cell lines SGC-7901,MKN-45, MKN-74. METHODS: Human gastric cancer lines SGC-7901,MKN-45, MKN-74 were treated with OM in the absenceand presence of NM-3. The inhibitory rates weredetected by MTT assay. Synergistic effect of OM andNM-3 on the growth of survivin, bcl-2, bax and p53 inSGC-7901 cells were examined by semiquantitative RT-PCR and Western blotting, and their growth inhibitoryeffects were also observed on SGC-7901 tumor xenograftin nude mice.RESULTS: OM combined with NM-3 exhibited asynergistic inhibitory effect on the growth of SGC-7901,MKN-45 and MKN-74 cells in a time-dependent manner.Twenty-four hours after treatment with OM, NM-3 aloneand their combination, mRNA expression of survivin andbcl-2 in SGC-7901 cells decreased, p53 mRNA expressionincreased. OM (4 g/L) combined with NM-3 significantlyincreased the expression of p53 mRNA and decreasedthe expression of survivin and bcl-2 compared witheither agent alone (193% ± 34% vs 129% ± 12%;44% ± 18% vs 92% ± 18%; 36 ± 17% vs 93% ± 23%,P < 0.05). Western blotting showed that the synergisticeffect of OM and NM-3 on protein translation of survivin,bcl-2 and p 53 was in accordance with their mRNAs.Furthermore, OM/NM-3 combination obviously exhibitedantitumor growth effect in xenografted human gastriccancer cells SGC-7901 compared with either agent alone.CONCLUSION: OM combined with NM-3 has synergisticinhibitory effects on human gastric cancer cells in vitro and can suppress the growth of xenografted human gastric cancer cells SGC-7901 in vivo. AIM: To investigate the synergistic effect of oxymatrine (OM) and angiogenesis inhibitor NM-3 on modulatingapoptosis in human gastric cancer cell lines SGC-7901, MKN-45, MKN-74. METHODS: Human gastric cancer lines SGC-7901, 45, MKN-74 were treated with OM in the absence and presence of NM-3. The inhibitory rates weredetected by MTT assay. Synergistic effect of OM andNM-3 on the growth of survivin, bcl-2, bax and p53 inSGC-7901 cells were examined by semiquantitative RT-PCR and Western blotting, and their growth inhibitory effects were also observed on SGC-7901 tumor xenograft nude mice. Results: OM combined with NM-3 exhibit asynergistic inhibitory effect on the growth of SGC-7901, MKN-45 and MKN-74 cells in a time-dependent manner. Twenty-four hours after treatment with OM, NM-3 alone and their combination, mRNA expression of survivin andbcl-2 in SGC-7901 cells decreased, p53 mRNA expressionincreased. OM / L) combined with NM-3 significantly increases the expression of p53 mRNA and d ecreased the expression of survivin and bcl-2 compared witheither agent alone (193% ± 34% vs 129% ± 12%; 44% ± 18% vs 92% ± 18%; 36 ± 17% vs 93% ± 23%, P < 0.05). Western blotting showed that the synergisticeffect of OM and NM-3 on protein translation of survivin, bcl-2 and p53 was in accordance with their mRNAs. Still Advanced, OM / NM-3 combination was demonstrated in vitro growth effect in xenografted human gastriccancer cells SGC-7901 compared with either agent alone. CONCLUSION: OM combined with NM-3 has synergistic inhibitory effect on human gastric cancer cells in vitro and can suppress the growth of xenografted human gastric cancer cells SGC-7901 in vivo.