脱氢姜酮对人肺癌细胞A549细胞毒活性的研究  

Studies on the Cytotoxicity of Dehydrozingerone in A549 Human Lung Cancer Cells

作　　者：张亚莉[1] 程宏明[1] 许鹏翔[1] 吴振[1,2] 

机构地区：[1]厦门大学化学化工学院化学生物学福建省重点实验室 [2]厦门大学医学院,福建厦门361005

出　　处：《厦门大学学报（自然科学版）》2010年第4期548-551,共4页Journal of Xiamen University：Natural Science

基　　金：国家自然科学基金(20732004)

摘　　要：对生姜中有效成分脱氢姜酮对人肺癌细胞A549细胞（简称A549细胞）毒活性进行研究,同时考察其氢化产物姜酮的细胞毒活性,研究其构效关系.实验利用MTT法测定脱氢姜酮和姜酮对A549细胞的生长抑制作用,DNA电泳研究脱氢姜酮和姜酮对DNA切割作用,免疫印迹实验检测相关蛋白的表达.实验结果表明：脱氢姜酮对A549细胞增殖具有一定的抑制作用,在40~300μmol/L之间呈剂量依赖性;脱氢姜酮抑制A549细胞增殖的能力和对DNA的切割能力大于姜酮;N-乙酰基-L-半胱氨酸（NAC）明显抑制脱氢姜酮的活性,对姜酮没有影响.免疫印迹结果显示脱氢姜酮可诱导CHOP蛋白的表达,表明脱氢姜酮通过内质网应急途径发挥作用.The mechanism of cytotoxicity by dehydrozingerone or zingerone in A549 human lung cancer cells was investigated. Cytotoxicity assay, DNA fragmentation assay and western blot analysis were performed. The results indicated that dehydrozingerone in the range of 40 μmol/L to 300 μmol/L inhibited A549 cell growth in a dose-dependent manner. In the presence of Cu（II）, both dehydrozingerone and zingerone caused breakage of supercoiled plasmid pBR322 DNA. Dehydrozingerone had a high DNA cleavage activity. NAC reversed dehydrozingerone-induced A549 cell death. Up-regulation of CHOP contributed to dehydrozingerone-induced A549 cell death. The ER stress pathway involving CHOP was activated in dehydrozingerone-induced A549 cell death.

关 键 词：脱氢姜酮 姜酮 A549细胞 抗肿瘤活性 

分 类 号：R739.5[医药卫生—肿瘤] R282.71[医药卫生—临床医学]