NM-3对体外胃癌细胞株SGC-7901的作用和机制探讨

目的：研究新小分子血管生成抑制剂NM-3对体外培养的胃癌SGC79n1细胞的作用，并探讨NM-3对胃癌抑制作用的机理。方法：将体外培养的人胃癌细胞株SGC7901用NM-3、卡铂及生理盐水处理，观察细胞的生长规律。并在不同时间段以流式细胞仪检测细胞的凋亡率，分析细胞周期分布。结果：将药物作用后1h，2h，3h，6h，12h，24h，48h，72h的胃癌SGC7901细胞通过流式细胞仪检测胃癌细胞早期凋亡率及凋亡峰。发现NM-3组（1mol／L）在72h内与对照组比较细胞早期调亡率无显著差异（P2〉0．05）；经0．1mol／L卡铂处理的细胞组早期即可诱导发生明显的凋亡，并随着时间的延长调亡率增高，呈时间依赖性，与对照组相比较，有显著差异（P〈0．05）。对细胞周期分布的分析中，NM-3组（1mg／L）Sub-G1峰与对照组比较无显著差异（P〉0．05）。而卡铂能使细胞周期发生相对变化，随着药物作用时间的增加，Go／G1期细胞增多，而S期覆G2／M期细胞则相应减少。结论：NM-3对胃癌组织的生长抑制主要是通过作用于血管内皮细胞，减少肿瘤新生血管生成。而对体外培养的人胃癌细胞无直接诱导其凋亡的作用。

The Effect of NM-3 on Cells Proliferation and Apoptosis of the Human Gastric Cancer Cell SGC-7901 in vitro

Objective: To study the action of NM3, which is a kind of angiogenesis inhibitor, on the growth and apoptosis of human gastric carcinoma cell line SGC-7901 and discuss its action mechanism. Methods:Human gastric carcinoma cell line SGC-7901 was treated with NM-3, Carboplatin and NS Cell proliferation was evaluated with MTT assay, Distributions of cell cycle and apoptosis rate were determined with flow cytometry, cell apoptosis was confirmed by morphology. Results:The inhibition effect of NM-3 was not apparent on the proliferation of SGC-7901 compared with controls, the apoptosis rate was not statistically different (P>0. 05). In cell cycle analysis, NM-3 could not increase the proportion of cells in the G0/G1 phase which was an indication of early apoptosis. Conclusion:NM-3 could not induce the apoptosis of human gastric cancer cell SGC-7901 in vitro, it enhanced the sensitivity of Carboplatin on human gasric cancer cell SGC-7901 in vitro. It had no direct effect on proliferation of gastric carcinoma cells. The anticancer mechanism of NM-3 in animal model was mainly related to its antiangiogenesis action.