Apoptosis induction of human gastric cancer SGC-7901 cells by oridonin and its mechanism

Objective To investigate the in vitro cell cycle arrest and apoptosis inducing effects of oridonin on SGC-7901 cell lines and the action mechanisms. Methods After administration of 10-80 μmol/L oridonin for 24-120 h, the CCK8 method was used to investigate the inhibitory effect of oridonin on SGC-7901 cells. Cell apoptosis and cell cycle arrest were investigated by flow cytometry (FCM). The ex-pression of apoptosis related proteins was detected using Western blotting. Results Oridonin could signifi-cantly inhibit the growth of SGC-7901 cells in both time-dependent and dose-dependent manners. FCM re-vealed that after treatment with different concentrations of ofidonin (0, 10, 40, 60, 80 μmol/L) for 24 h, the nnmber of G_2/M stage cells was (9.90±1.17)%, (9.94±0.27)%, (11.76±0. 16)%, (15.64± 1.48)%, (22.59 ± 1.01)%, and that of S stage cells was (31.79 ±1.03)%, (30.90±0.47)%, (29. 25 ± 0. 80 ) %, (21.46 ±1.61 ) %, (18. 81± 0.61 ) % respectively. The apoptotic rate was (9. 92± 0.56)%, (12.78±1.54)% and (20.62±2.39)% respectively within 0, 12 and 24 h after treatment with 80 μmol/L oridonin. With the extension of oridonin treatment, the bcl-2 protein expression in SGG-7901 cells was gradually reduced, and pro-caspase 3 was activated. Conclusion Oridonin can induce ap-optosis and G_2/M cell cycle arrest in SGC-7901 cells, which was probably contributed to the down-regula-tion of protein bcl-2 as well as activation of caspase-3. Key words: Oridonin;  Gastric carcinoma;  Cell cycle;  Apoptosis;  Caspases