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首页> 外文期刊>Integrative cancer therapies. >Chan-Yu-Bao-Yuan-Tang, the Water Extract of a Chinese Medicine Prescription, Induces S-Phase Arrest and Mitochondria-Mediated Apoptosis in Human Lung Adenocarcinoma Cells
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Chan-Yu-Bao-Yuan-Tang, the Water Extract of a Chinese Medicine Prescription, Induces S-Phase Arrest and Mitochondria-Mediated Apoptosis in Human Lung Adenocarcinoma Cells

机译:Chan-Yu-Bao-Yuan-Tang,一种中药处方的水提取物,在人肺腺癌细胞中诱导S期阻滞和线粒体介导的凋亡。

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Previous clinical studies have shown good efficacy of the traditional Chinese medicinal herbal water extract Chan-Yu-Bao-Yuan-Tang (CYBYT) in lung cancer patients. In this study, CYBYT’s effects on proliferation and apoptosis of human lung adenocarcinoma cell line SPC-A-1 cultured in vitro were explored. An XTT assay, cell cycle analysis, Annexin V-FITC staining and Western blot were applied to identify the viability of cells, cell cycle arrest, stages of apoptosis, and signaling proteins, respectively. The results showed that CYBYT inhibited the growth of SPC-A-1 cells by reducing the cells in G0/G1 phase but increasing them in S phase in a concentration-dependent manner, and inducing apoptosis, whereas it had no significant inhibitory effects on the normal human IMR-90 fibroblasts. Furthermore, early and total induction of apoptosis was positively correlated with the concentration of CYBYT in SPC-A-1 cells, and the rate of total apoptosis was greater in the CYBYT 100 μg/mL and 50 μg/mL groups than that of the positive control 5-fluorouracil (5-Fu) group. Moreover, CYBYT upregulated bax, cleaved caspase-3 protein expression, downregulated bcl-2 protein expression, and released mitochondrial cytochrome c into the cytosol in a time- and concentration-dependent manner. Our findings indicated that CYBYT could significantly inhibit growth and induce apoptosis via the mitochondrial pathway in human lung adenocarcinoma cell line SPC-A-1.
机译:先前的临床研究表明,中草药水提取物禅玉宝元汤(CYBYT)在肺癌患者中具有良好的疗效。在这项研究中,研究了CYBYT对体外培养的人肺腺癌细胞SPC-A-1增殖和凋亡的影响。应用XTT分析,细胞周期分析,膜联蛋白V-FITC染色和Western印迹分别鉴定细胞的活力,细胞周期停滞,凋亡阶段和信号蛋白。结果表明,CYBYT通过抑制G0 / G1期的细胞,但以浓度依赖的方式增加S期的细胞并诱导细胞凋亡,从而抑制了SPC-A-1细胞的生长,但对SPC-A-1细胞没有明显的抑制作用。正常人IMR-90成纤维细胞。此外,凋亡的早期诱导和完全诱导与SPC-A-1细胞中CYBYT的浓度呈正相关,CYBYT组100μg/ mL和50μg/ mL的总凋亡率比阳性组高。对照5-氟尿嘧啶(5-Fu)组。此外,CYBYT以时间和浓度依赖性方式上调bax,切割caspase-3蛋白表达,下调bcl-2蛋白表达,并将线粒体细胞色素c释放到细胞质中。我们的发现表明,CYBYT可以通过人肺腺癌细胞SPC-A-1的线粒体途径显着抑制其生长并诱导凋亡。

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