中国临床药理学杂志
中國臨床藥理學雜誌
중국림상약이학잡지
The Chinese Journal of Clinical Pharmacology
2015年
20期
2031-2033
,共3页
氮芥衍生物%抗肿瘤%凋亡%caspase
氮芥衍生物%抗腫瘤%凋亡%caspase
담개연생물%항종류%조망%caspase
nitrogen mustard derivative%antitumor%apoptosis%caspase
目的:体外评价N-4-(二氯乙基)丁胺-1,8-萘酰亚胺( XHH)对HepG2细胞的抑制作用及其作用机制。方法采用MTT法检测细胞增殖,高内涵筛选分析仪结合Annexin V-FITC/Hoechst33342, PI/Hoechst33342和Rh123/Hoechst33342双染色法检测细胞形态及膜电位;免疫荧光法检测caspase-3, caspase-9, Bcl-2, Bax的表达水平。结果 XHH能抑制HepG2细胞增殖,诱导细胞凋亡,降低线粒体膜电位,提高Bax/Bcl-2,使caspase-3, caspase-9表达增加。结论 XHH具有较好的抗HepG2肿瘤细胞作用,可通过线粒体途径诱导细胞凋亡。
目的:體外評價N-4-(二氯乙基)丁胺-1,8-萘酰亞胺( XHH)對HepG2細胞的抑製作用及其作用機製。方法採用MTT法檢測細胞增殖,高內涵篩選分析儀結閤Annexin V-FITC/Hoechst33342, PI/Hoechst33342和Rh123/Hoechst33342雙染色法檢測細胞形態及膜電位;免疫熒光法檢測caspase-3, caspase-9, Bcl-2, Bax的錶達水平。結果 XHH能抑製HepG2細胞增殖,誘導細胞凋亡,降低線粒體膜電位,提高Bax/Bcl-2,使caspase-3, caspase-9錶達增加。結論 XHH具有較好的抗HepG2腫瘤細胞作用,可通過線粒體途徑誘導細胞凋亡。
목적:체외평개N-4-(이록을기)정알-1,8-내선아알( XHH)대HepG2세포적억제작용급기작용궤제。방법채용MTT법검측세포증식,고내함사선분석의결합Annexin V-FITC/Hoechst33342, PI/Hoechst33342화Rh123/Hoechst33342쌍염색법검측세포형태급막전위;면역형광법검측caspase-3, caspase-9, Bcl-2, Bax적표체수평。결과 XHH능억제HepG2세포증식,유도세포조망,강저선립체막전위,제고Bax/Bcl-2,사caspase-3, caspase-9표체증가。결론 XHH구유교호적항HepG2종류세포작용,가통과선립체도경유도세포조망。
Objective To investigate the effects of 2-(4-di(2-chlo-roethyl) aminobutylamino)-1H-benz-[de]isoquinoline-1,3(2H)-dione( XHH) , a novel nitrogen mustard derivative, on the growth and apoptosis in human hepatoma HepG2 cells in vitro.Methods Cell pro-liferative effect was assessed by MTT assay.Changes of morphology and mitochondrial membrane potential ( MMP) were assessed by AnnexinV-FITC/Hoechst33342 , PI/Hoecsht33342 and Rh123/Hoechst33342 double staining using high content screening ( HCS ) .The expression of caspase-3 , caspase-9 , Bcl-2 , Bax was assessed by immunofluores-cence method using HCS. Results The results indicated that XHH could inhibit the proliferation of HepG2 cells, induce apoptosis, lose MMP, up-regulate the ratio of Bax/Bcl-2, increase the expression of caspase-3 , caspase-9.Conclusion XHH could inhibit proliferative of human hepatoma HepG2 cells and induce cell apoptosis via mitochon-drial pathway.