| Kinase Assay: |
| Integrative Medicine Research, 2015,May 4(1):76-7. | | Vitisin B stimulates osteoblastogenesis via estrogen receptor-mediated pathway[Reference: WebLink] |
METHODS AND RESULTS:
Vitisin B stimulates osteoblastogenesis via estrogen receptor-mediated pathway | | Drug Chem Toxicol. 2013 Jul;36(3):313-9. | | Cytotoxicity of (-)-vitisin B in human leukemia cells.[Pubmed: 23030068 ] | Vitis thunbergii var. taiwaniana (VTT) is an indigenous Taiwanese wild grape and is used as a folk medicine in Taiwan. VTT is rich in polyphenols, especially quercetin and resveratrol derivatives, which were demonstrated to exhibit inhibitory activities against carcinogenesis and prevent some neurodegenerative diseases. (-)-Vitisin B is one of the resveratrol tetramers extracted from VTT. In this study, we investigated the mechanisms of (-)-Vitisin B on the induction of apoptosis in human HL-60 promyelocytic leukemia cells.
METHODS AND RESULTS:
First, (-)-Vitisin B significantly inhibited cell proliferation through inducing cell apoptosis. This effect appeared to occur in a time- and dose-dependent manner. Cell-cycle distribution was also examined, and we found that (-)-Vitisin B significantly induced a sub-G1 population in a dose-dependent manner. In addition, (-)-Vitisin B exhibited stronger inhibitory effects on cell proliferation than resveratrol. Second, (-)-Vitisin B dose dependently induced apoptosis-related protein expressions, such as the cleavage form of caspase-3, caspase-8, caspase-9, poly(ADP ribose) polymerase, and the proapoptotic Bax protein. Third, (-)-Vitisin B treatment also resulted in increases in c-Jun N-terminal kinase (JNK) phosphorylation and Fas ligand (FasL) expression. Moreover, the (-)-Vitisin B-induced FasL expression and caspase-3 activation could be reversed by a JNK inhibitor.
CONCLUSIONS:
These results suggest that (-)-Vitisin B-induced apoptosis of leukemia cells might be mediated through activation of JNK and Fas death-signal transduction. |
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