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首页> 外文期刊>Life sciences >Acetone extract of Angelica sinensis inhibits proliferation of human cancer cells via inducing cell cycle arrest and apoptosis.
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Acetone extract of Angelica sinensis inhibits proliferation of human cancer cells via inducing cell cycle arrest and apoptosis.

机译：当归丙酮提取物通过诱导细胞周期停滞和凋亡来抑制人类癌细胞的增殖。

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摘要

Angelica sinensis (Oliv.) Diels, a traditional Chinese medicine, has been widely prescribed in treatment of gynecological diseases. Bio-based assays for extracts of Angelica sinensis showed that the acetone extract (AE-AS) had dose-dependently antiproliferative effect on A549, HT29, DBTRG-05MG and J5 human cancer cells. The IC50 values of AE-AS on mentioned cancer cells ranged from 35 to 50 microg/ml after 24 h of treatment. After 72 h of exposure, AE-AS (40 microg/ml) significantly reduced A549 cell proliferation to 24 +/- 3.2% of control. In A549 cells, the cell cycle analysis showed that AE-AS induced a significant increase in the number of cells in G0/G1, with a concomitant decrease in the number of cells in S phase. AE-AS-induced chromatin changes and apoptosis of A549 cells were confirmed by Hoechst 33342 DNA staining and annexin V staining. A549 cells treated with AE-AS caused activation of caspase-9 and -3, and AE-AS-induced apoptosis could be inhibited by the broad-spectrum caspase inhibitor, z-VAD-fmk. The Western blot indicated the AE-AS-triggered apoptosis is mediated via suppression of Bcl-2 oncoprotein expression rather than p53 or Bax. Besides, AE-AS decreased the levels of cdk4 protein was observed. These results indicate that the AE-AS could induce G1/S arrest and activate the mechanism of apoptosis in human cancer cells. Extracts obtained from different methods of fractionation might possess distinct bioactivity. These results prompted us to further evaluate the in vivo anticancer effects and elucidate the chemical composition profile of AE-AS.
机译：当归Diels是一种传统中药，已广泛用于治疗妇科疾病。当归提取物的生物基测定表明，丙酮提取物（AE-AS）对A549，HT29，DBTRG-05MG和J5人癌细胞具有剂量依赖性的抗增殖作用。治疗24小时后，AE-AS对上述癌细胞的IC50值在35至50微克/毫升之间。暴露72小时后，AE-AS（40μg/ ml）将A549细胞增殖显着降低至对照的24 +/- 3.2％。在A549细胞中，细胞周期分析表明，AE-AS诱导了G0 / G1细胞数量的显着增加，同时伴随着S期细胞数量的减少。 Hoechst 33342 DNA染色和膜联蛋白V染色证实了AE-AS诱导的A549细胞染色质变化和凋亡。 AE-AS处理的A549细胞引起caspase-9和-3的活化，而广谱caspase抑制剂z-VAD-fmk可以抑制AE-AS诱导的细胞凋亡。 Western印迹表明，AE-AS触发的凋亡是通过抑制Bcl-2癌蛋白表达而不是p53或Bax介导的。此外，观察到AE-AS降低了cdk4蛋白的水平。这些结果表明，AE-AS可以诱导G1 / S阻滞并激活人癌细胞的凋亡机制。从不同的分馏方法获得的提取物可能具有独特的生物活性。这些结果促使我们进一步评估体内抗癌作用并阐明AE-AS的化学组成特征。

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