Dihydromyricetin reduced Bcl-2 expression via p53 in human hepatoma HepG2 cells.
Dihydromyricetin reduced Bcl-2 expression via p53 in human hepatoma HepG2 cells.
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DOI：
10.1371/journal.pone.0076886
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发表时间：
2013
期刊：
影响因子：
3.7
通讯作者：
Zhu R
中科院分区：
文献类型：
--
作者：
Wu S;Liu B;Zhang Q;Liu J;Zhou W;Wang C;Li M;Bao S;Zhu R
二氢杨梅素（DHM）是黄酮类化合物的主要活性成分。根据我们以前的数据，它具有抗癌活性，并诱导人肝癌HepG 2细胞凋亡。在这项研究中，我们研究了p53是否参与DHM触发的癌细胞活力抑制和凋亡诱导。采用MTT法检测DHM对HepG 2细胞增殖的影响。同时采用小分子干扰RNA（siRNA）沉默p53基因的表达。Western blot检测p53、Bax/Bcl-2蛋白表达。细胞计数结果显示DHM能有效抑制HepG 2细胞的生长，并呈时间和剂量依赖性。DHM处理后P53蛋白表达明显增加，而Bcl-2蛋白表达明显降低。此外，在与Pifithrin-α（PFT-α，p53抑制剂）共同处理后，Bcl-2表达被逆转。p53基因沉默后Bax表达无明显变化。这些结果明确并支持了DHM通过p53信号通路上调Bax/Bcl-2表达诱导人肝癌HepG 2细胞凋亡的新功能。
Dihydromyricetin (DHM) is a major active ingredient of flavonoids compounds. It exhibited anticancer activity and induced apoptosis in human hepatocellular carcinoma HepG2 cells according to our previous data. In this study, we investigated whether p53 is involved in DHM-triggered viability inhibition and apoptosis induction in cancer cells. MTT [3-(4, 5-Dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide] assay was employed to evaluate the viability of HepG2 cells after DHM treatment. Meanwhile, p53 small interfering RNA (siRNA) was adopted to silence p53 expression. Protein level of p53 and Bax/Bcl-2 were evaluated by western blot analysis. Cell counting assay showed that DHM inhibited HepG2 cell growth effectively in a time- and dose-dependent manner. P53 expression was significantly increased after DHM treatment, whereas Bcl-2 was reduced potently. Furthermore, after co-treatment with Pifithrin-α (PFT-α, p53 inhibitor), Bcl-2 expression was reversed. The expression of Bax was no significant change, which was also observed after p53 silence. These findings defined and supported a novel function that DHM could induce human hepatocellular carcinoma HepG2 cells apoptosis by up-regulating Bax/Bcl-2 expression via p53 signal pathway.
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