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目的:探讨SW体外诱导人胃癌细胞株SGC7901凋亡的机制。方法:应用MTT法确定SW对体外培养的SGC7901细胞的作用剂量,通过流式细胞术及凋亡相关调控基因p53、cmyc、Bcl2的检测对细胞凋亡及细胞周期的测定,观察SW对胃癌细胞SGC7901增殖周期的影响以及抑制肿瘤细胞增殖的方式,同时利用激光共聚焦显微镜对细胞内Ca2+浓度的监测,研究SW与细胞内Ca2+超载的关系。结果:SW体外抗SGC7901细胞的完全致死剂量为6.2μg·ml-l,高于0.05μg·ml-l时抑制作用明显(P<0.05),其LC50为0.84μg·ml-l;经SW0.5～1.5μg·ml-l处理24h可引起凋亡抑制基因p53、Bcl2的明显下降、凋亡促进基因cmyc的明显升高以及肿瘤细胞内Ca2+超载,最终诱导SGC7901细胞凋亡。实验还证实SW主要作用于肿瘤细胞的S期,使瘤细胞主要积聚在S期。结论:SW通过多种途径诱导细胞凋亡可能是其发挥抗癌作用的重要机制。
Objective: To investigate the mechanism of SW apoptosis in vitro induced by human gastric cancer cell line SGC7901. Methods: The effect of SW on the SGC7901 cells cultured in vitro was determined by MTT method. The apoptosis and cell cycle of SGC7901 cells were detected by flow cytometry and p53, cmyc and Bcl2 genes. The effects of SW on gastric cancer cells SGC7901 proliferation cycle and the inhibition of tumor cell proliferation, meanwhile, the laser scanning confocal microscopy was used to monitor intracellular Ca2 + concentration and the relationship between SW and intracellular Ca2 + overload. Results: The complete lethal dose of SW in vitro against SGC7901 cells was 6.2μg · ml-1, and the inhibitory effect was significantly higher than 0.05μg · ml-1 (P <0.05). The LC50 of SW was 0.84μg · ml-1. Treatment with 5 ~ 1.5μg · ml-1 for 24 hours caused a significant decrease of apoptosis-suppressing genes p53 and Bcl2, a significant increase of cmyc, and over-loading of Ca2 + in tumor cells, finally inducing apoptosis of SGC7901 cells. Experiments also confirmed that SW mainly acts on the S phase of tumor cells, so that tumor cells mainly accumulate in S phase. CONCLUSIONS: SW induces apoptosis in a variety of ways and may be an important mechanism of its anti-cancer effect.