靛红衍生物IF203通过线粒体途径诱导人肝癌HepG2细胞凋亡  

IF203 induced apoptosis in human liver HepG2 cells through mitochondrial pathway

作　　者：尚应辉[1] 孟书聪[1] 王明群[1] 董晓敏[1] 张页[1] 肖军军[1] 

机构地区：[1]北京大学基础医学院细胞生物学系,北京市100191

出　　处：《解剖学报》2011年第3期340-344,共5页Acta Anatomica Sinica

基　　金：教育部教育振兴行动计划专项资助项目(985-2-016-24)

摘　　要：目的探讨靛红衍生物IF203诱导人肝癌HepG2细胞凋亡及线粒体凋亡途径。方法体外培养HepG2细胞,应用倒置相差显微镜观察细胞形态变化;采用酸性磷酸酶法(APA)、流式细胞术(FCM)和免疫印迹法(Western blotting),检测IF203对HepG2细胞生长、细胞凋亡率、线粒体膜电位、Caspase-9、Caspase-3、细胞色素C表达的影响。结果不同浓度IF203作用24h和48h时可抑制HepG2细胞生长;光镜下观察10mg/L IF203作用24h时HepG2细胞变圆、固缩;IF203诱导HepG2细胞凋亡率增加;IF203可以引起HepG2细胞线粒体平均荧光强度显著降低;凋亡相关基因蛋白Caspase-9表达下调,Caspase-3表达下调,细胞色素C表达上调。结论 IF203抑制人肝癌HepG2细胞的增殖,通过干预线粒体途径诱导HepG2细胞发生凋亡。Objective To study the involvement of mitochondrial pathway in IF203 induced apoptosis in human liver HepG2 cells. Methods HepG2 cells were cultured in DMEM containing 10% fetal bovine serum at 37℃ in a humidified atmosphere with 5% CO2. Inverted phase contrast microscope was used to detect the morphologic changes ; Acid phosphatase assay （APA） , flow cytometry （FCM）and Western blotting were used to detect the changes of cell viability, apoptosis ratio, mitochondrial transmembrane potential, the expressions of apoptosis-related protein Caspase-9, Caspase-3 and cytochrome C. Results Cell growth was inhibited after HepG2 ceils were co-cultured with different concentration of IF203 for 24 hours and 48 hours. HepG2 cells showed round and shrank after they were co-cultured with IF203 of 10 mg/ L. Apoptosis ratios caused by IF203 were increased. Mean fluorescence intensity （MFI） of mitochondrial transmembrane potentials in HepG2 ceils decreased. The expressions of apoptosis-related protein Caspase-9 and Caspase-3 decreased, but the cytochrome C expression increased. Conclusion IF203 could significantly restrain cell growth of liver cancer cell line HepG2. IF203 can activate mitochondrial signaling pathway which would induce apoptosis, but the mechanism is yet to be studied in detail.

关 键 词：吲哚满酮类化合物 线粒体膜电位 免疫印迹法 HEPG2细胞 

分 类 号：R730.5[医药卫生—肿瘤]