Study the molecular mechanisms of (-)-vitisin B on the induction of apoptosis in human leukemia cells

• Main Authors: Yueh-E Lo, 駱月娥
• Other Authors: 梁有志
• Format: Others
• Language: zh-TW
• Published: 2009
• Online Access: http://ndltd.ncl.edu.tw/handle/76897278126606646818

碩士 === 臺北醫學大學 === 醫學科學研究所 === 97 === Abstract Vitis thunbergii var. taiwaniana (VTT) is a Taiwan original wild grape, and has been used as a folk medicine in Taiwan. VTT is rich in polyphenols, especially quercetin and resveratrol’s derivatives, which have been demonstrated that exhibited an inhibitory activity on the carcinogenesis and prevented some of neurodegenerative diseases. (-)-vitisin B is a resveratrol’s derivative and extracted from VTT. In this study, we have investigated the mechanisms of (-)-vitisin B on the induction of apoptosis in human HL-60 promyelocytic leukemia cells. First, we found that (-)-vitisin B significantly inhibited cell proliferation and induced cell apoptosis. This effect appears to occur in a time- and dose-dependent manner. Cell cycle distribution was also examined and found that (-)-vitisin B significantly induced SubG1 population in a dose-dependent manner. In addition, (-)-vitisin B markedly increased the cell cycle population in S and G2/M phases at 6.25?嵱. These results indicated that (-)-vitisin B might alter cell cycle distribution in HL-60 cells. When analyzing the expression of cell apoptosis-related proteins, we found that (-)-vitisin B dose-dependently induced PARP cleavage, activated caspase-3, -8, and -9, and increased proapoptotic bax protein expression. Moreover, (-)-vitisin B treatment also resulted in the increase of phosphorylation of JNK and p38, and FasL expression. These results suggest that (-)-vitisin B -induced cell apoptosis might be mediated through the activation of JNK and p38 and Fas death signal transduction.