Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/62140
標題: Induction of apoptosis by the anthocyanidins through regulation of Bcl-2 gene and activation of c-Jun N-terminal kinase cascade in hepatoma cells
作者: Yeh, C.T.
顏國欽
Yen, G.C.
關鍵字: anthocyanidin;apoptosis;HepG(2) cell;JNK pathway;Bcl-2 family;caspase-3;hepatocellular-carcinoma;lipid-peroxidation;cyanidin;3-o-beta-d-glucoside;elderberry anthocyanins;nh2-terminal kinase;mediated apoptosis;protein-kinases;in-vitro;delphinidin;inhibition
Project: Journal of Agricultural and Food Chemistry
期刊/報告no:: Journal of Agricultural and Food Chemistry, Volume 53, Issue 5, Page(s) 1740-1749.
摘要: 
Anthocyanidins that are reddish pigments widely distributed in fruit and vegetables have been reported to possess antioxidant and anticancer activities. To understand the molecular basis of the putative anticancer activity of anthocyanidins, we investigated the antiproliferation effects of anthocyanidins in human hepatoma cell lines. Delphinidin, cyanidin, and malvidin exhibited strong growth inhibitory effects against human hepatoma HepG(2), but were less effective against Hep3B. According to the appearance of the caspase-3 fragments and stimulated proteolytic cleavage of poly (ADP-ribose) polymerase (PARP) in time-dependent studies, delphinidin induced apoptotic cell death characterized by intern ucleosomal DNA fragmentation and caused a rapid induction of caspase-3 activity. RT-PCR and Western blot data revealed that delphinidin stimulated an increase in the c-Jun and JNK phosphorylation expression at mRNA and protein levels, respectively. Moreover, delphinidin-induced apoptotic cell death was accompanied by up-regulation of Bax and down-regulation of Bcl-2 protein. Dephinidin-induced DNA fragmentation was blocked by N-acetyl-L-cysteine and catalase, suggesting that the death signaling was triggered by oxidative stress. Our experiments provide evidence that delphinidin is an effective apoptosis inducer in HepG2 cells through regulation of Bcl-2 family moleculars and activation of c-Jun N-terminal kinase cascade. The results suggest that induction of apoptosis by anthocyanidins is a pivotal mechanism of their cancer chemopreventive functions.
URI: http://hdl.handle.net/11455/62140
ISSN: 0021-8561
DOI: 10.1021/jf048955e
Appears in Collections:食品暨應用生物科技學系

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