期刊
ARCHIVES OF TOXICOLOGY
卷 83, 期 2, 页码 121-129出版社
SPRINGER HEIDELBERG
DOI: 10.1007/s00204-008-0337-3
关键词
Antrodia camphorata (AC); Death receptor (DR); Histone acetylation; Nuclear factor kappa B (NF kappa B); Trichostatin A (TSA); Zhankuic acid A
类别
资金
- National Science Council, Taiwan
The endemic species of Antrodia camphorate (AC) is a promising chemotherapeutic drug for cancer. We found that the ethanol extract from wild fruiting bodies of Antrodia camphorata (EEAC) could induce HL 60 cells apoptosis via histone hypoacetylation, up-regulation of histone deacetyltransferase 1 (HDAC 1), and down-regulation of histone acetyltransferase activities including GCN 5, CBP and PCAF in dose-dependent manner. In combination with histone deacetylase inhibitor, trichostatin A (TSA), did not block EEAC-induced apoptosis. Interestingly, combined treatment (100 nM of TSA and 100 mu g/ml EEAC) caused synergistic inhibition of cell growth and increase of apoptotic induction. EEAC could effectively increase the cytotoxic sensitivity of TSA through the up-regulation of DR5 and NF kappa B activation. In this present study, bioassay-guided fractionation of EEAC led to a major active compound, zhankuic acid A, as the bioactive marker. Moreover, our findings may represent an experimental basis for developing EEAC as a potential chemotherapeutic adjuvant.
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