中药癌痛克对人胃癌细胞SGC-7901增殖、凋亡作用及机制研究

目的通过观察不同浓度癌痛克对胃癌细胞株SGC-7901增殖及凋亡的作用，以及在相应状态下细胞内视网膜母细胞瘤（Rb）基因相对表达量的改变，探讨中药癌痛克的抗胃癌作用机制。方法以不同浓度癌痛克作用SGC-7901细胞，CCK-8检测细胞增殖抑制率，流式细胞术检测细胞凋亡率细胞周期，RT—PCR方法检测细胞内Bcl-2基因表达变化。结果2～50μg／ml癌痛克可抑制SGC-7901细胞增殖并诱导其凋亡，其抑制及诱导凋亡效应呈浓度依赖性；细胞周期分析处于G1期细胞百分比明显增多，处于G2／M期的细胞减少，Rb基因mRNA表达上调。结论中药癌痛克可通过抑制SGC-7901细胞增殖或诱导其凋亡，且其机制可能通过上调Rb基因表达途径使细胞阻滞在G1期，进而诱导细胞凋亡。

Effect of Aitongke on proliferation, apoptosis of human gastric cancer cells SGC-7901 and its mechanisms

Objective To investigate the anti-cancer mechanisms ofaitongke, its impact on proliferation, apoptosis and its underlying mechanisms in human gastric cancer cells SGC-7901. Methods SGC-7901 cells were treated by aitongke of different concentrations, the proliferating rate, the apoptosis rate, cell cycle and retinoblastoma （Rb） gene mRNA level change of SGC-7901 cells were evaluated by CCK method, flow eytometry analysis and RT-PCR method respectively. Results Aitongke （2-50mg/L） could effectively inhibited SGC-7901 cell proliferation and induced cell apoptosis, both with a time-dose dependent manner. Cells accumulated in the gap 1 （G1） phases, while reduced in the gap 2 and mitosis（G2/M） phases of the cell cycle, and the apoptosis peak significantly occurred. Aitongke could upregulate the expression of Rb gene, and with a dose dependent manner. Conclusion Aitongke has a potential role on anti-gastric cancer by inhibiting proliferation of SGC-7901 cell, as well as inducing cell apoptosis. And the apoptosis-inducing mechanism is mediated through the G1 blocking of cell cycle in SGC-7901 cells involved with the up-regulating expression of Rb gene.