Objective: To investigate the effects of curcumin combined with thalidomide on the proliferation and apoptosis of acute myeloid leukemia KG-1 cells, and its correlation with B-cell lymphoma-xL (Bcl-xL), signal transducer and activator of transcription 3 (STAT3).
Methods: MTT assay was used to detect the proliferation of KG-1 cells and screen the optimal combined concentration of curcumin and thalidomide. The effects of curcumin, thalidomide and their combination on the proliferation and apoptosis of KG-1 cells were analyzed by MTT method and flow cytometry, respectively. The mRNA expression levels of STAT3 and Bcl-xL in single-drug group, two-drug combination group and control group (untreated cells) were detected by real-time quantitative PCR.
Results: Both curcumin and thalidomide inhibited the proliferation of KG-1 cells in a concentration-dependent manner in the range of 20-100 μmol/L (r =0.657, r =0.681). The IC50 value of curcumin and thalidomide at 48 h was (42.07±0.50) μmol/L and (57.01±2.39) μmol/L, respectively. The cell proliferation inhibition rate of curcumin (40 μmol/L) + thalidomide (60 μmol/L) was (86.67±1.53)%, which was significantly higher than (51.67±1.15)% of curcumin (40 μmol/L) and (55.33±1.53)% of thalidomide (60 μmol/L) (both P < 0.05). Treated with curcumin and thalidomide alone or in combination, the apoptosis rate of KT-1 cells was (18.67±2.08)%, (21.33±2.52)%, and (46.67±1.53)%, respectively, which was significantly higher than (0.72±0.03)% of control group (all P < 0.05). The cell apoptosis rate of two-drug combination group was significantly higher than that of single-drug group (both P < 0.05). Compared with the control group, the mRNA expressions of STAT3 and Bcl-xL in single-drug group, two-drug combination group were significantly decreased (both P < 0.05). Compared with single-drug group, the mRNA expressions of STAT3 and Bcl-xL in two-drug combination group were also significantly decreased (both P < 0.05).
Conclusion: Curcumin combined with thalidomide can synergistically down-regulate the expression of STAT3 and Bcl-xL, inhibit the proliferation of KG-1 cells, and induce apoptosis.
题目: 姜黄素联合沙利度胺抑制KG-1细胞增殖及相关作用机制研究.
目的: 探讨姜黄素联合沙利度胺对急性髓系白血病KG-1细胞增殖、凋亡的影响及与抗凋亡蛋白（Bcl-xL）、信号转导和转录激活因子3（STAT3）的关系。.
方法: MTT法检测KG-1细胞增殖，筛选姜黄素、沙利度胺的最佳联合浓度；分别采用MTT法、流式细胞术分析姜黄素、沙利度胺单药及两药联用对KG-1细胞增殖、凋亡的影响；实时定量PCR检测单药组、两药联用组、对照组（未处理细胞）的 STAT3、Bcl-xL mRNA表达水平。.
结果: 姜黄素和沙利度胺在20-100 μmol/L范围内对KG-1细胞增殖的抑制作用均呈浓度依赖性（r =0.657，r =0.681）。姜黄素在作用48 h 的IC50值为（42.07±0.50）μmol/L，沙利度胺为（57.01±2.39）μmol/L。姜黄素（40 μmol/L）+沙利度胺（60 μmol/L）两药联用的细胞增殖抑制率为（86.67±1.53）%，明显高于单用姜黄素的（51.67±1.15）%和单用沙利度胺的（55.33± 1.53）%（均P <0.05）。姜黄素、沙利度胺单药及两药联用作用48 h，KG-1细胞凋亡率分别为（18.67±2.08）%、（21.33± 2.52）%和（46.67±1.53）%，明显高于对照组的（0.72±0.03）%（均P <0.05）；两药联用组KG-1细胞凋亡率亦明显高于两药单药组（均P <0.05）。与对照组比较，姜黄素、沙利度胺单药组及两药联用组 STAT3、Bcl-xL mRNA表达均显著下降（均P <0.05）；与姜黄素、沙利度胺单药组比较，两药联用组STAT3、Bcl-xL mRNA表达亦显著下降（均P <0.05）。.
结论: 姜黄素联合沙利度胺可协同下调STAT3与Bcl-xL表达，抑制KG-1细胞增殖，诱导KG-1细胞凋亡。.
Keywords: B-cell lymphoma-xL; acute myeloid leukemia; curcumin; signal transducer and activator of transcription 3; thalidomide.