首页> 美国卫生研究院文献>Experimental and Therapeutic Medicine >Green tea catechin epigallocatechin-3-gallate attenuates the cell viability of human non-small-cell lung cancer A549 cells via reducing Bcl-xL expression
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Green tea catechin epigallocatechin-3-gallate attenuates the cell viability of human non-small-cell lung cancer A549 cells via reducing Bcl-xL expression

机译:绿茶儿茶素epigallocatechin-3-gallate通过降低Bcl-xL表达来减弱人非小细胞肺癌A549细胞的细胞活力

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摘要

Clinical and epidemiological studies have indicated that the consumption of green tea has a number of beneficial effects on health. Epigallocatechin-3-gallate (EGCg), the major polyphenolic compound present in green tea, has received much attention as an active ingredient. Among the numerous promising profiles of EGCg, the present study focused on the anticancer effects. Apoptosis induced by EGCg and subsequent cell growth suppression have been demonstrated in a number of cell culture studies. However, the underlying mechanism of apoptotic cell death remains unclear. Thus, the aim of the present study was to identify the major molecule that mediates proapoptotic cell death by EGCg. The effect of EGCg on cell proliferation and the induction of mRNA that modulates apoptotic cell death was evaluated in the A549 human non-small-cell lung cancer cell line. In addition, morphological changes were assessed by microscopy in A549 cells that had been treated with 100 μM EGCg for 24 h. The MTT assay revealed that cell proliferation was significantly reduced by EGCg in a dose-dependent manner (3–100 μM). The mRNA expression level of B-cell lymphoma-extra large (Bcl-xL) was decreased in A549 cells following 24 h incubation with 100 μM EGCg. Therefore, the results indicated that the inhibition of cell proliferation by EGCg may be achieved via suppressing the expression of the cell death-inhibiting gene, Bcl-xL.
机译:临床和流行病学研究表明,食用绿茶对健康有许多有益影响。绿茶中存在的主要多酚类化合物Epigallocatechin-3-gallate(EGCg)作为有效成分已引起了广泛关注。在EGCg的众多前景广阔的研究中,本研究的重点是抗癌作用。在许多细胞培养研究中已经证明了由EGCg诱导的凋亡和随后的细胞生长抑制。但是,凋亡细胞死亡的潜在机制仍不清楚。因此,本研究的目的是鉴定介导EGCg促凋亡细胞死亡的主要分子。在A549人非小细胞肺癌细胞系中评估了EGCg对细胞增殖的影响以及调节凋亡细胞死亡的mRNA的诱导作用。另外,通过显微镜在已经用100μMEGCg处理24小时的A549细胞中评估了形态变化。 MTT分析表明,EGCg以剂量依赖的方式(3–100μM)显着降低了细胞增殖。与100μMEGCg孵育24小时后,A549细胞中B细胞淋巴瘤超大型(Bcl-xL)的mRNA表达水平降低。因此,结果表明,可以通过抑制细胞死亡抑制基因Bcl-xL的表达来实现EGCg对细胞增殖的抑制。

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