摘要目的:探讨西达本胺联合三氧化二砷（As 2O 3）对T细胞淋巴瘤Hut-78细胞增殖的抑制作用及机制。 方法:分别应用1.0 μmol/L西达本胺、4.0 μmol/L As 2O 3、1.0 μmol/L西达本胺+4.0 μmol/L As 2O 3（低浓度）和1.5 μmol/L西达本胺、6.0 μmol/L As 2O 3、1.5 μmol/L西达本胺+6.0 μmol/L As 2O 3（高浓度）处理Hut-78细胞24 h或48 h，采用四甲基偶氮唑盐（MTT）法检测各药物处理组Hut-78细胞增殖情况并计算增殖抑制率，采用蛋白质印迹法检测各药物处理组Hut-78细胞bcl-2蛋白和血管内皮生长因子（VEGF）蛋白的表达。 结果:1.0 μmol/L西达本胺、4.0 μmol/L As 2O 3、1.0 μmol/L西达本胺+ 4.0 μmol/L As 2O 3处理Hut-78细胞24 h时，细胞增殖抑制率分别为（8.8±0.1）%、（9.2±0.5）%、（11.0±0.1）%（ F=12.45， P<0.05）；处理48 h时，细胞增殖抑制率分别为（19.1±0.5）%、（18.3±0.9）%、（23.1±1.3）%（ F=9.86, P<0.05）。1.5 μmol/L西达本胺、6.0 μmol/L As 2O 3、1.5 μmol/L西达本胺+ 6.0 μmol/L As 2O 3处理Hut-78细胞24 h时，细胞增殖抑制率分别为（15.4±0.9）%、（13.2±0.9）%、（18.2±1.1）%（ F=7.06， P<0.05）；处理48 h时，细胞增殖抑制率分别为（28.5±1.2）%、（31.3±0.8）%、（45.2±2.1）%（ F=14.32， P<0.05）。1.0 μmol/L西达本胺、4.0 μmol/L As 2O 3、1.0 μmol/L西达本胺+ 4.0 μmol/L As 2O 3处理Hut-78细胞24 h时，bcl-2蛋白相对表达量分别为（58.4±2.9）%、（55.9±3.8）%、（53.2±2.1）%（ F=17.52， P<0.05），VEGF蛋白相对表达量分别为（60.5±4.2）%、（57.5±2.8）%、（50.9±3.5）%（ F=7.36， P<0.05）。处理48 h时，细胞bcl-2蛋白相对表达量分别为（48.2±1.8）%、（40.1±2.2）%、（32.3±3.1）%（ F=10.38, P<0.05），VEGF蛋白相对表达量分别为（51.4±4.1）%、（48.9±2.9）%、（40.8±3.8）%（ F=8.96, P<0.05）。1.5 μmol/L西达本胺、6.0 μmol/L As 2O 3、1.5 μmol/L西达本胺+ 6.0 μmol/L As 2O 3处理Hut-78细胞24 h时，bcl-2蛋白相对表达量分别为（55.4±3.1）%、（42.5±2.8）%、（37.8±4.2）%（ F=10.35， P<0.05），VEGF蛋白相对表达量分别为（49.2±3.4）%、（42.1±4.9）%、（34.3±5.1）%（ F=17.82， P<0.05）；处理48 h时，bcl-2蛋白相对表达量分别为（40.1±0.9）%、（35.3±1.6）%、（27.8±2.4）%（ F=15.36， P<0.05），VEGF蛋白相对表达量分别为（40.3±3.8）%、（35.9±4.6）%、（20.1±2.9）%（ F=9.78， P<0.05）。 结论:西达本胺和As 2O 3对T细胞淋巴瘤Hut-78细胞具有协同抑制作用，可能与bcl-2、VEGR表达下调有关。

abstractsObjective:To investigate the effect of chidamide combined with arsenic acid on the proliferation inhibitory of T cell lymphoma Hut-78 cells and its mechanism.Methods:Low concentration group included 1.0 μmol/L chidamide, 4.0 μmol/L arsenic trioxide or both of them (1.0 μmol/L chidamide + 4.0 μmol/L arsenic trioxide). High concentration group included 1.5 μmol/L chidamide, 6.0 μmol/L arsenic trioxide or both of them (1.5 μmol/L chidamide + 6.0 μmol/L arsenic trioxide). Both groups were used to treat Hut-78 cells for 24 h and 48 h, respectively. Cell proliferation of Hut-78 cells in all drug treatment groups was tested by using methyl thiazolyl tetrazolium (MTT) method, and the proliferation inhibitory rate was also calculated. The expressions of vascular endothelial growth factor (VEGR) and bcl-2 protein of Hut-78 cells in different drug treatment groups by using Western blotting.Results:The cell proliferation inhibitory rate of Hut-78 cells treated for 24 h of 1.0 μmol/L chidamide, 4.0 μmol/L arsenic trioxide or both of them (1.0 μmol/L chidamide+ 4.0 μmol/L arsenic trioxide) was (8.8±0.1)%, (9.2±0.5)% and (11.0±0.1)%, respectively ( F = 12.45, P < 0.05); The cell proliferation inhibitory rate of Hut-78 cells treated for 48 h was (19.1±0.5)%, (18.3±0.9)%, (23.1±1.3)%, respectively ( F = 9.86, P < 0.05). The cell proliferation inhibitory rate of Hut-78 cells treated for 24 h of 1.5 μmol/L chidamide, 6.0 μmol/L arsenic trioxide or both of them (1.5 μmol/L chidamide+ 6.0 μmol/L arsenic trioxide) was (15.4±0.9)%, (13.2±0.9)% and (18.2±1.1)%, respectively ( F = 7.06, P < 0.05); The cell proliferation inhibitory rate of Hut-78 cells treated for 48 h was (28.5±1.2)%, (31.3±0.8)%, (45.2±2.1)%, respectively ( F = 14.32, P < 0.05). When Hut-78 cells were treated with 1.0 μmol/L chidamide, 4.0 μmol/L arsenic trioxide or both of them (1.0 μmol/L chidamide+ 4.0 μmol/L arsenic trioxide) for 24 h, the relative expression level of bcl-2 protein was (58.4±2.9)%, (55.9±3.8)%, (53.2±2.1)%, respectively ( F = 17.52, P < 0.05); the relative expression level of VEGF protein was (60.5±4.2)%, (57.5±2.8)%, (50.9±3.5)%, respectively ( F = 7.36, P < 0.05). When Hut-78 cells were treated with 1.0 μmol/L chidamide, 4.0 μmol/L arsenic trioxide or both of them (1.0 μmol/L chidamide+ 4.0 μmol/L arsenic trioxide) for 48 h, the relative expression level of bcl-2 protein was (48.2±1.8)%, (40.1±2.2)%, (32.3±3.1)%, respectively ( F = 10.38, P < 0.05); the relative expression level of VEGF protein was (51.4±4.1)%, (48.9±2.9)%, (40.8±3.8)%, respectively ( F = 8.96, P < 0.05). When Hut-78 cells were treated with 1.5 μmol/L chidamide, 6.0 μmol/L arsenic trioxide or both of them (1.5 μmol/L chidamide+ 6.0 μmol/L arsenic trioxide) for 24 h, the relative expression level of bcl-2 protein was (55.4±3.1)%, (42.5±2.8)%, (37.8±4.2)%, respectively ( F= 10.35, P < 0.05); the relative expression level of VEGF protein was (49.2±3.4)%, (42.1±4.9)%, (34.3±5.1)%, respectively ( F= 17.82, P <0.05). When Hut-78 cells were treated with 1.5 μmol/L chidamide, 6.0 μmol/L arsenic trioxide or both of them (1.5 μmol/L chidamide+ 6.0 μmol/L arsenic trioxide) for 48 h, the relative expression level of bcl-2 protein was (40.1±0.9)%, (35.3±1.6)%, (27.8±2.4)%, respectively ( F = 15.36, P < 0.05); the relative expression level of VEGF protein was (40.3±3.8)%, (35.9±4.6)%, (20.1±2.9)%, respectively ( F = 9.78, P < 0.05). Conclusion:Chidamide and arsenic trioxide have synergistic inhibitory effects on T cell lymphoma Hut-78 cells, which may be related to the down-regulated expressions of bcl-2 and VEGR.