黑龙江大学自然科学学报
黑龍江大學自然科學學報
흑룡강대학자연과학학보
JOURNAL OF NATURAL SCIENCE OF HEILONGJIANG UNIVERSITY
2011年
5期
708-716
,共9页
吴振%张冲%薛识%张亚莉%方美娟%丘鹰昆
吳振%張遲%薛識%張亞莉%方美娟%丘鷹昆
오진%장충%설식%장아리%방미연%구응곤
3-芳基-α,β-不饱和酮%NAC%迈克尔加成%细胞凋亡
3-芳基-α,β-不飽和酮%NAC%邁剋爾加成%細胞凋亡
3-방기-α,β-불포화동%NAC%매극이가성%세포조망
3 - aryl α,β - unsaturated ketone%NAC%Michael adduct%apoptosis
选择了与3-芳基-α,β-不饱和酮结构关联的六个天然产物,研究了3-芳基-α,β-不饱和酮在诱导人肺癌细胞A549凋亡的作用与分子机制.结果表明,六个天然产物的细胞毒活性来源于3-芳基-α,β-不饱和酮结构,缺失该结构,活性明显降低;NAC明显抑制3-芳基-α,β-不饱和酮诱导的细胞毒活性,3-芳基-α,β-不饱和酮诱导的A549细胞凋亡涉及迈克尔加成、内质网应急和线粒体依赖的细胞凋亡分子机理.
選擇瞭與3-芳基-α,β-不飽和酮結構關聯的六箇天然產物,研究瞭3-芳基-α,β-不飽和酮在誘導人肺癌細胞A549凋亡的作用與分子機製.結果錶明,六箇天然產物的細胞毒活性來源于3-芳基-α,β-不飽和酮結構,缺失該結構,活性明顯降低;NAC明顯抑製3-芳基-α,β-不飽和酮誘導的細胞毒活性,3-芳基-α,β-不飽和酮誘導的A549細胞凋亡涉及邁剋爾加成、內質網應急和線粒體依賴的細胞凋亡分子機理.
선택료여3-방기-α,β-불포화동결구관련적륙개천연산물,연구료3-방기-α,β-불포화동재유도인폐암세포A549조망적작용여분자궤제.결과표명,륙개천연산물적세포독활성래원우3-방기-α,β-불포화동결구,결실해결구,활성명현강저;NAC명현억제3-방기-α,β-불포화동유도적세포독활성,3-방기-α,β-불포화동유도적A549세포조망섭급매극이가성、내질망응급화선립체의뢰적세포조망분자궤리.
Six natural products were applied to investigate the mechanism that the 3 -aryl α,β-unsaturated ketone induced human lung cancer A549 cell apoptosis.The effects of these compounds with or without the structure of 3 - aryl α,β - unsaturated ketone on human lung cancer A549 cells by the MTT assay were examined.It is found that these natural products with a fragment of 3 -aryl α,β- unsaturated ketone,including curcumin (CUR),chalcone (CC) and dehydrozingerone (DHZ),were cytotoxic,with CUR > CC > DHZ,whereas the compounds without the 3 - aryl α,β - unsaturated ketone including tetrahydrocurcumin (THC),dihydrochalcone (DHCC) and zingerone (ZG) were not.In vitro,3 - aryl α,β - unsaturated ketone formed Michael adducts with the thiol nucleophile N - acethlcysteine.In cultured cells,preincubation of the NAC with CUR,CC and DHZ decreased the cytotoxicity significantly except the THC,DHCC and ZG.Moreover,CUR and DHZ induced A549 cell apoptosis by activating the proteins JNK,P-JNK,CHOP,Bcl-2,Bax and cyto-c.These results suggested that 3 - aryl α,β - unsaturated ketone mediated cell apoptosis involve in the mechanism of Michael adduct formation and induction of endoplasmic reticulum stress in human lung cancer A549 cells.