中文摘要：

目的研究芳姜黄酮衍生物（ATD）对人皮肤黑色素瘤WM35细胞增殖及凋亡的影响,并探讨其作用机制。方法不同浓度（5~80μmol/L）ATD体外作用WM35细胞。CCK-8法检测增殖抑制率;AO/EB染色、倒置显微镜观察细胞凋亡形态;DNA片段化检测细胞凋亡;比色法检测Caspase-3酶活性;流式细胞术检测细胞凋亡;Western blotting检测Bax及Bcl-2蛋白表达。结果 ATD对WM35细胞有增殖抑制作用,呈时间-剂量依赖性（P〈0.05）。ATD诱导WM35细胞凋亡,呈剂量依赖性（P〈0.05）,Caspase-3酶活性随药物浓度增加而增强（P〈0.05）。随药物浓度增加,Bax/Bcl-2比值逐渐升高。结论 ATD对WM35细胞有抑制增殖及促凋亡作用,其机制是使凋亡相关蛋白Bax表达上调、Bcl-2表达下调,激活细胞凋亡途径关键酶Caspase-3,进而抑制肿瘤细胞分化与增殖。

英文摘要：

Objective To investigate the effect of ar-turmerone derivatives（ ATD） on proliferation and apoptosis in human melanoma WM35 cells,and to explore its mechanism. Methods WM35 cells were incubated with different concentrations of ATD（ 5-80 μmol / L） in vitro. Cell proliferation was measured by cell counting kits（ CCK-8） assay. The cell morphology of WM35 was observed by inverted microscope after AO / EB staining. Apoptosis was detected by DNA fragmentation. Caspase-3 cellular activities were measured by a colorimetric method. The apoptosis rate was analyzed by flowcytometry. The expression of apoptosis associated protein,Bcl-2 and Bax,in WM35 cells were examined byWestern blotting. Results ATD exhibited obvious proliferation inhibition effect on the growth of WM35 cells in a time-and-dose dependent manner（ P〈0. 05）. Meanwhile,ATD exhibited an apoptosis-inducing effect on WM35 cells in a drug-and-dose dependent manner（ P〈0. 05）. Expression of Bax increased while Bcl-2 decreased with the increase of the concentration of ATD（ P〈0. 05）. Conclusion ATD exhibites marked effect of proliferation inhibition and apoptosis-inducing on WM35 cells. ATD activates the apoptosis pathway of key enzyme. The apoptosis associated protein Bax is up-regulated while that of Bcl-2 is down-regulated,which may be the mechanism of ATD in affecting the proliferation and differentiation of tumors.