二甲基胂酸抑制胃癌细胞增殖的研究

Study on the Inhibition of Dimethylarsinic Acid on SGC7901 Gastric Cancer Cell Proliferation

目的:探讨二甲基胂酸(DMAA)对SGC7901胃癌细胞增殖的抑制作用及其可能的机制。方法:依次用5,10,15,20,25,30mmol/L二甲基胂酸处理培养的SGC7901胃癌细胞24hrs,在5mmol/L和10mmol/L的浓度下分别处理6,12,18,24,30,36,42,48hrs,用MTT计数法测定DMAA对肿瘤细胞增殖的抑制率,用激光共聚焦显微镜检测细胞形态变化以及用DNA凝胶电泳检测细胞凋亡。结果:DMAA在不同浓度下对肿瘤细胞的抑制作用呈现典型的双曲线,即随着浓度的增加DMAA对胃癌细胞的抑制率不断增加并逐渐趋于稳定;在形态学上DMAA在低浓度下引起胃癌细胞的胞膜出泡、核固缩、染色体断裂和凋亡小体等典型的细胞凋亡的变化,而在高浓度下主要引起细胞坏死;DNA凝胶电泳结果显示,在低浓度DMAA作用下胃癌细胞DNA呈现细胞凋亡的梯状带型,而在高浓度下梯状带型则消失。结论:DMAA抑制胃癌细胞的增殖,其在低浓度时能有效诱导胃癌SGC7901细胞凋亡,而在高浓度时使胃癌细胞坏死而死亡。

Objective： To investigate the inhibition roles of dimethylarsinic acid （DMAA） on cultured SGC7901 gastric cancer cells and its possible mechanisms. Methods： The cultured SGC7901 gastric cancer cells were treated with 5, 10, 15, 20, 25 and 30mmol/L concentrations of DMAA. The cytotoxicity caused by DMAA was assessed by MTT assay. The morphological changes caused by DMAA were detected under laser confocal microscope. The formation of nuclear fragmentation and nuclear bodies were analyzed by gel electrophoresis. Results： The cytotoxicity of DMAA on SGC7901 gastric cancer cells increased along with the increase of the concentra- tion of DMAA. Morphological changes caused by low concentration of DMAA were observed, including condensation of cellular chro- matin, nuclear fragmentation and apoptotic bodies. High concentration of DMAA mainly caused the neorobiosis. And gel analysis also showed that the fragmentation of internucleosomal DNA was apparent when the concentration of DMAA was below 5 mmol/L, but disappeared above 10 mmol/L. Conclusion： It is concluded that DMAA can cause the death of SGC7901 gastric cancer cells mainly via apoptosis at low concentration but primarily necrosis at high concentration.