中文摘要：

目的研究三氧化二砷（arsenic trioxde，As2O3）诱导体外培养鸡马立克病（Marek disease，MD）肿瘤细胞株MDCC—MSB1细胞凋亡的机制。方法将体外培养的MDCC—MSB1根据加As2O3终浓度不同分为0（对照）、2、4、8μmol／L组。As2O3作用48h后，用四甲基偶氮唑盐比色法（MTr）检测As2O3对MDCC—MSB1的抑制作用，采用荧光显微镜观察细胞形态学变化，琼脂糖凝胶电泳DNA梯形带检测细胞凋亡，罗丹明123（Rhodamine 123）染色流式细胞术检测线粒体膜电位（△ψm）的变化。结果随As2O3水平增加（0、2、4、8μmol／L），其抑制率逐渐升高，分别为0、（5．34±3．02）％、（10．78±0．55）％、（20．02±3．24）％，任意两组间的比较差异有统计学意义（P〈0．01）；各组细胞凋亡指数逐渐增高，分别为3．200±0．459、11．543±0．391、17．206±0．636、21．343±0．620，任意两组间的比较差异有统计学意义（P〈0．01）；4组均出现典型的DNA Ladder，同时细胞膜完整，但线粒体△ψm下降（PI-／Rh123-）的凋亡细胞增加，增加率分别为（1．06±0．14）％、（4．63±0．04）％、（9．62±0．07）％和（10．39±0．10）％，任意两组间的比较差异有统计学意义（P〈0．01）。结论As2O3可诱导MDCC—MSB1细胞凋亡，其诱导凋亡的途径与△ψm降低有关。

英文摘要：

Objective To investigate the mechanism of apoptosis induced by arsenic trioxide（As2O3） on MDCC-MSB1 cancer cell line in vitro. Methods MDCC-MSB1 cells were divided into 4 groups, treated with 0 （control, group）, 2, 4 or 8 μmol/L of As2O3. At 48 h following the treatment, MTT assay was applied to detect the inhibitory effect of As2O3 on MDCC-MSB1. Morphological changes of apoptosis were observed by fluorescence microscopy. Apoptosis was examined by DNA Ladder. Changes of mitochondrial transmembrane potential were examined by Rhodamin 123 dye and flow cytometry. Results Inhibition ratio was 0, （5.34 ± 3.02）%, （10.78 ± 0.55）% and （20.02 ± 3.24）% respectively, along with the dosages of As2O3, the differences between the groups were statistically significant（P 〈 0.01 ）. Morphologic changes of apoptosis were observed by DNA ladder of agarose gel electrophoresis. Apoptosis rates were significantly increased from 3.200 ± 0.459, 11.543 ± 0.391, 17.206 ± 0.636 to 21.343 ± 0.620, and the differences between the groups were statistically significant（P 〈 0.01 ）. DNA ladder of experimental group was detected. Intact cell membrane, and mitochondrial transmembrane potential PI-/Rh123- decreased apoptotic cells percentage was significantly increased from （1.06 ± 0.14）%, （4.63 ± 0.04）%, （9.62 ± 0.07 ）% to （10.39 ± 0.10）%, respective to doses of 0, 2,4, and 8 μmol of As2O3. The differences between the groups were statistically significant（P 〈 0.01 ）. Conclusions As2O3 can induce apoptosis in MDCC-MSB1 cells by decreasing the mitochondrial transmembrane potential.