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目的探讨甲硫氨酸(Met)及其联合化疗药物对胃癌细胞凋亡的诱导作用。方法将人胃癌细胞株SGC-7901分别置于6种不同培养液:含L-Met、含D-Met、不含Met而替以同型半胱氨酸(Met-Hcy+)或在上述培养液中分别加入氟尿嘧啶(5-Fu)。培养48h后,应用流式细胞仪检测细胞凋亡率及凋亡相关基因bcl-2和bax的表达,并在电镜下观察细胞形态变化。结果无论是否加入化疗药物,D-Met组的细胞凋亡率均高于Met-Hcy+组和L-Met组;L-Met加5-Fu组的细胞凋亡率显著高于L-Met组和Met-Hcy+组,但与D-Met组差异无显著性意义。各组间的bcl-2和bax表达率无改变。结论D-Met及D-Met联合化疗药物可通过诱导胃癌细胞凋亡而抑制肿瘤生长,作用机制可能与bcl-2和bax的表达无关。
Objective To investigate the induction of methionine (Met) and its combination with chemotherapeutics on gastric cancer cell apoptosis. Methods Human gastric cancer cell line SGC-7901 was placed in 6 different culture media: L-Met, D-Met, Met-free and Met-Hcy + Fluorouracil (5-Fu) was added separately. After cultured for 48 hours, the apoptosis rate and the expression of apoptosis-related genes bcl-2 and bax were detected by flow cytometry. The morphological changes of cells were observed under electron microscope. Results The apoptosis rate of D-Met group was higher than that of Met-Hcy + group and L-Met group with or without chemotherapeutic drugs. The apoptosis rate of L-Met plus 5-Fu group was significantly higher than that of L-Met group and L-Met group Met-Hcy + group, but no significant difference with D-Met group. There was no change in the expression of bcl-2 and bax between groups. Conclusion D-Met and D-Met combined with chemotherapy can inhibit tumor growth by inducing apoptosis of gastric cancer cells. The mechanism may be related to the expression of bcl-2 and bax.