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目的探讨柠檬酸钠(sodium citrate,CT)与三氧化二砷(As_2O_3,,AS)联合应用对胃癌SGC-7901细胞凋亡及作用机制。方法用sodium citrate(终浓度为5 mmol/L,CT5)和As_2O_3(终浓度依次为5 μmol/L,AS5)处理体外传代培养的胃癌SGC-7901细胞株。应用DAPI细胞核染色和流式细胞仪检测细胞凋亡和细胞周期的变化;RT-PCR法观察抗凋亡相关基因bcl-2表达的变化。结果 sodium citrate与As_2O_3联合应用相对于单用sodium citrate或As_2O_3可显著提高诱导胃癌细胞凋亡率(P<0.05);与空白组相比,用药后G_0/G_1期细胞比例下降,G_2/M期细胞比例上升,细胞周期阻滞于G_2/M期,抗凋亡基因bcl-2表达明显下降。结论 sodium citrate与As_2O_3联合应用具有协同抗胃癌细胞的作用,其机制可能与细胞周期阻滞、增强诱导胃癌细胞凋亡以及调控凋亡相关基因的表达有关。
Objective To investigate the apoptosis and its mechanism of gastric cancer SGC-7901 cells treated by combination of sodium citrate (CT) and arsenic trioxide (As 2 O 3, AS). Methods SGC-7901 gastric cancer cell lines were cultured in vitro with sodium citrate (5 mmol / L, CT5) and As2O3 (5 μmol / L final concentration, AS5) The changes of apoptosis and cell cycle were detected by DAPI staining and flow cytometry. The expression of anti-apoptosis-related gene bcl-2 was detected by RT-PCR. Results Compared with blank control group, the combination of sodium citrate and As_2O_3 could significantly increase the apoptosis rate of gastric cancer cells (P <0.05) compared with that of sodium citrate alone or As_2O_3 alone. Compared with the blank control group, the percentage of cells in G_0 / The proportion of cells increased, cell cycle arrest in G2 / M phase, the expression of anti-apoptotic gene bcl-2 decreased significantly. Conclusion The combination of sodium citrate and As_2O_3 has synergistic effect on gastric cancer cells. The mechanism may be related to cell cycle arrest, enhanced apoptosis of gastric cancer cells and regulation of apoptosis related genes.