摘要
目的探讨西达本胺联合三氧化二砷(As2O3)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1.0μmol/L西达本胺、4.0μmol/L As2O3、1.0μmol/L西达本胺+4.0μmol/L As2O3(低浓度)和1.5μmol/L西达本胺、6.0μmol/L As2O3、1.5μmol/L西达本胺+6.0μmol/L As2O3(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1.0μmol/L西达本胺、4.0μmol/L As2O3、1.0μmol/L西达本胺+4.0μmol/L As2O3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)。1.5μmol/L西达本胺、6.0μmol/L As2O3、1.5μmol/L西达本胺+6.0μmol/L As2O3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)。1.0μmol/L西达本胺、4.0μmol/L As2O3、1.0μmol/L西达本胺+4.0μmol/L As2O3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)。1.5μmol/L西达本胺、6.0μmol/L As2O3、1.5μmol/L西达本胺+6.0μmol/L As2O3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
Objective 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 1.0μmol/L chidamide,4.0μmol/L arsenic trioxide or both of them(1.0μmol/L chidamide+4.0μmol/L arsenic trioxide).High concentration group included 1.5μmol/L chidamide,6.0μmol/L arsenic trioxide or both of them(1.5μmol/L chidamide+6.0μmol/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 1.0μmol/L chidamide,4.0μmol/L arsenic trioxide or both of them(1.0μmol/L chidamide+4.0μmol/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 1.5μmol/L chidamide,6.0μmol/L arsenic trioxide or both of them(1.5μmol/L chidamide+6.0μmol/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 1.0μmol/L chidamide,4.0μmol/L arsenic trioxide or both of them(1.0μmol/L chidamide+4.0μmol/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
作者
王共爱
李晴
郝云良
董沙沙
Wang Gongai;Li Qing;Hao Yunliang;Dong Shasha(Department of Hematology,Jining NO.1 People's Hospital,Jining 272100,China;Department of Internal Medicine,Jining Rencheng District People's Hospital,Jining 272000,China)
出处
《白血病．淋巴瘤》
CAS
2020年第5期257-260,共4页
Journal of Leukemia & Lymphoma
