目的研究新型有机锡化合物DBDCT对肝细胞HL02的毒性作用及其机制。方法 MTT法测定DBDCT对HL02细胞活力的影响,计算IC50,并于光学显微镜下观察细胞形态的改变;紫外分光光度法测定LDH的释放量;流式细胞术测定细胞凋亡与细胞周期;Western blot测定周期蛋白Cdc2的表达。结果 DBDCT可抑制HL02细胞的增殖,且随着药物浓度的增加,细胞形态逐渐模糊、细胞固缩变圆,表现出明显的细胞毒性;24 h IC50为5.77μmol/L;DBDCT可引起LDH的大量释放,并将细胞阻滞于G2/M期,细胞凋亡率增加,且呈现明显的量效关系;细胞周期蛋白依赖性激酶Cdc2的表达则随着给药浓度的增加而降低。结论 DBDCT可通过改变细胞膜的通透性,降低Cdc2的表达,引起G2/M期细胞阻滞与细胞凋亡,进而产生明显的肝细胞毒性。 Objective To study the toxic effect of novel organotin compound DBDCT on hepatocyte HL02 and its mechanism. Methods MTT method was used to determine the effect of DBDCT on the viability of HL02 cells. IC50 was calculated and observed under optical microscope. The release of LDH was measured by UV spectrophotometry. Apoptosis and cell cycle were measured by flow cytometry. The expression of cyclin Cdc2 was determined. Results DBDCT could inhibit the proliferation of HL02 cells. With the increase of drug concentration, the morphology of cells gradually became fuzzy and the cell shrinkage became round, showing obvious cytotoxicity. IC50 was 5.77 μmol / L at 24 h. DBDCT could cause a large number of LDH Release, and the cells arrested in G2 / M phase, the rate of apoptosis increased, and showed a significant dose-effect relationship; Cdk2 expression of cyclin-dependent kinase decreased with increasing concentration. Conclusion DBDCT can reduce the expression of Cdc2, change the cell membrane permeability, cause cell arrest and apoptosis in G2 / M phase, and then induce obvious hepatotoxicity.