异异甘草素抑制人非小细胞肺癌a549细胞增殖,诱导细胞凋亡。

IF 2.4 4区 医学 Q3 PHARMACOLOGY & PHARMACY
Ya-Ling Hsu, Po-Lin Kuo, Lien-Chai Chiang, Chun-Ching Lin
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引用次数: 72

摘要

1. 异异黄酮素(ISL)是一种天然色素,具有简单的查尔酮结构4,2',4'-三羟基查尔酮。在本研究中,我们首次报道了is诱导的对人非小细胞肺癌A549细胞系增殖的抑制作用。2. 结果表明,ISL不仅能抑制A549细胞增殖,还能诱导细胞凋亡,阻断G1期细胞周期进程。ELISA实验表明,ISL显著增加p53和p21/WAF1蛋白的表达,导致细胞周期阻滞。3.Fas及其两种配体,即膜结合Fas配体(mFasL)和可溶性Fas配体(sFasL)的增强可能是ISL诱导细胞凋亡的原因。4. 综上所述,p53和Fas/FasL凋亡系统可能参与了ISL在A549细胞中的抗增殖活性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Isoliquiritigenin inhibits the proliferation and induces the apoptosis of human non-small cell lung cancer a549 cells.

1. Isoliquiritigenin (ISL) is a natural pigment with the simple chalcone structure 4,2',4'-trihydroxychalcone. In the present study, we report, for the first time, ISL-induced inhibition of the proliferation of the human non-small cell lung cancer A549 cell line. 2. The results showed that ISL not only inhibited A549 cell proliferation, but also induced apoptosis and blocked cell cycle progression in the G1 phase. An ELISA assay demonstrated that ISL significantly increased the expression of p53 and p21/WAF1 protein, which caused cell cycle arrest. 3. An enhancement in Fas and its two ligands, namely membrane-bound Fas ligand (mFasL) and soluble Fas ligand (sFasL), may be responsible for the apoptotic effect induced by ISL. 4. Taken together, the results indicate that the p53 and Fas/FasL apoptotic system may participate in the antiproliferative activity of ISL in A549 cells.

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来源期刊
Clinical and Experimental Pharmacology and Physiology
Clinical and Experimental Pharmacology and Physiology PHARMACOLOGY & PHARMACY-PHYSIOLOGY
自引率
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发文量
128
期刊介绍: Clinical and Experimental Pharmacology and Physiology is an international journal founded in 1974 by Mike Rand, Austin Doyle, John Coghlan and Paul Korner. Our focus is new frontiers in physiology and pharmacology, emphasizing the translation of basic research to clinical practice. We publish original articles, invited reviews and our exciting, cutting-edge Frontiers-in-Research series’.
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