中文摘要：

目的探讨姜黄素衍生物——联氨基姜黄素（hydrazinocurcumin,HC）通过抑制STAT3（signal transduction and activators of transcription-3）信号通路对乳腺癌细胞MDA-MB-231侵袭迁移性的影响。方法以人乳腺癌细胞株MDA-MB-231为研究对象,分DMSO对照组和HC处理组。采用MTT法检测HC对MDA-MB-231乳腺癌细胞的生长抑制作用,刘氏染色检测细胞形态学改变,Transwell小室检测细胞侵袭能力,细胞划痕试验检测细胞迁移能力,Western blot检测STAT3、p-STAT3、MMP-9及MMP-2的蛋白表达水平。结果 MTT检测显示,HC处理的细胞生长受到抑制,其抑制率呈时间-剂量依赖关系;刘氏染色发现处理细胞形态发生改变,细胞变圆;Transwell小室检测显示对照组穿膜细胞数为（598.00±21.28）/视野,而10、20μmol/LHC处理后透膜细胞数分别为（94.00±6.56）/视野和（4.00±1.00）/视野,穿膜细胞数显著低于对照组（P〈0.05）;划痕试验表明对照组划痕闭合率约为54%,而10、20μmol/LHC处理组基本无闭合（P〈0.05）;Westernblot检测显示,不同浓度HC处理MDA-MB-231细胞后,p-STAT3明显降低,而总STAT3水平无明显差异,MMP-9、MMP-2的表达也有减少。结论 HC可以通过抑制STAT3的活化（即p-STAT3）,降低MMP-9、MMP-2的蛋白表达水平,从而抑制乳腺癌细胞MDA-MB-231的侵袭迁移性。

英文摘要：

Objective To investigate the effect of curcumin derivant（hydrazinocurcumin,HC） on the invasion and migration of human breast cancer of MDA-MB-231 cells through inhibiting STAT3 signal pathway.Methods Human breast cancer MDA-MB-231 cells were divided into 3 groups,control group,10 and 20 μmol/L HC treatment groups.Growth inhibition was measured with MTT assay.Morphological changes were detected by Liu staining.Cell invasion was measured by Transwell chamber,and migration of the cells was measured with scratch assay.Expressions of STAT3,p-STAT3,MMP-9,and MMP-2 were detected by Western blot analysis.Results After treated with HC,the proliferation of MDA-MB-231 cells was inhibited in a time and dose-depending manner.Liu staining demonstrated that the cell morphology had been changed,and became round in shape.The invasion assay showed the number of treated MDA-MB-231 cells was lower than those of control（94.00±6.56 and 4.00±1.00 vs 598.00±21.28,P0.05）.Scratch assay also showed the treated cells were inhibited.Western blot analysis demonstrated that the expressions of p-STAT3,MMP-9 and MMP-2 were decreased,while total STAT3 had no significant difference compared with control.Conclusion HC inhibits the invasion and migration of the human breast cancer of MDA-MB-231 cells,probably by inhibiting STAT3 activity,and then reducing MMP-9 and MMP-2 expressions.