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首页> 外文期刊>Archives of Toxicology >Active extracts of wild fruiting bodies of Antrodia camphorata (EEAC) induce leukemia HL 60 cells apoptosis partially through histone hypoacetylation and synergistically promote anticancer effect of trichostatin A
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Active extracts of wild fruiting bodies of Antrodia camphorata (EEAC) induce leukemia HL 60 cells apoptosis partially through histone hypoacetylation and synergistically promote anticancer effect of trichostatin A

机译：樟芝野生子实体的有效提取物（EEAC）通过组蛋白低乙酰化部分诱导白血病HL 60细胞凋亡，并协同促进曲古抑菌素A的抗癌作用

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摘要

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 μg/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 NFκB 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.
机译：樟脑樟脑（AC）的特有物种是一种有前途的癌症化学治疗药物。我们发现，樟芝野生子实体（EEAC）的乙醇提取物可以通过组蛋白低乙酰化，组蛋白脱乙酰基转移酶1（HDAC 1）的上调以及组蛋白乙酰转移酶活性的下调（包括GCN 5）诱导HL 60细胞凋亡。 CBP和PCAF呈剂量依赖性。与组蛋白脱乙酰基酶抑制剂合用，曲古抑菌素A（TSA）不能阻止EEAC诱导的细胞凋亡。有趣的是，联合处理（100 nM TSA和100​​μg/ ml EEAC）引起细胞生长的协同抑制和凋亡诱导的增加。 EEAC可通过上调DR5和NFκB激活来有效提高TSA的细胞毒性敏感性。在本研究中，EEAC的生物测定指导分馏产生了一种主要的活性化合物，詹库酸A，作为生物活性标记。此外，我们的发现可能代表开发EEAC作为潜在的化学治疗佐剂的实验基础。

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