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连苯三酚通过阻滞细胞周期和触发凋亡来抑制人肺腺癌A549细胞的生长。

Pyrogallol inhibits the growth of human pulmonary adenocarcinoma A549 cells by arresting cell cycle and triggering apoptosis.

作者信息

Han Yong Hwan, Kim Suhn Hee, Kim Sung Zoo, Park Woo Hyun

机构信息

Department of Physiology, Medical School, Institute for Medical Sciences, Centers for Healthcare Technology Development, Chonbuk National University, JeonJu, Republic of Korea.

出版信息

J Biochem Mol Toxicol. 2009 Jan-Feb;23(1):36-42. doi: 10.1002/jbt.20263.

Abstract

Pyrogallol (PG) is a polyphenol compound and has been known to be an O(2)(-) generator. We evaluated the effects of PG on the growth of human pulmonary A549 cells in relation to the cell cycle and apoptosis. Treatment with 50 or 100 microM PG significantly inhibited the cell growth of A549 for 72 h. DNA flow cytometric analysis indicated that PG slightly induced a G1 phase arrest of the cell cycle at 24 or 48 h, but did not induce the specific cell cycle arrest at 72 h. Intracellular GSH depletion was observed in PG-treated cells. PG induced apoptosis in A549 cells, as evidenced by sub-G1 cells, annexin V staining cells, and the loss of mitochondrial membrane potential (DeltaPsi(m)). The intracellular ROS (reactive oxygen species) level including O(2)(-) increased in PG-treated A549 cells at 24 and 48 h, and persisted at 72 h. The changes in GSH as well as ROS levels by PG affected the cell viability in A549 cells. In conclusion, PG inhibited the growth of human pulmonary A549 cells by inducing cell cycle arrest as well as triggering apoptosis.

摘要

连苯三酚(PG)是一种多酚化合物,已知它是一种超氧阴离子(O₂⁻·)生成剂。我们评估了PG对人肺A549细胞生长的影响,及其与细胞周期和细胞凋亡的关系。用50或100微摩尔/升的PG处理72小时可显著抑制A549细胞的生长。DNA流式细胞术分析表明,PG在24或48小时时轻微诱导细胞周期的G1期阻滞,但在72小时时未诱导特异性细胞周期阻滞。在PG处理的细胞中观察到细胞内谷胱甘肽(GSH)耗竭。PG诱导A549细胞凋亡,表现为亚G1期细胞、膜联蛋白V染色细胞以及线粒体膜电位(ΔΨm)丧失。在24和48小时时,PG处理的A549细胞内包括超氧阴离子(O₂⁻·)在内的活性氧(ROS)水平升高,并在72小时时持续存在。PG引起的GSH以及ROS水平变化影响了A549细胞的活力。总之,PG通过诱导细胞周期阻滞以及触发细胞凋亡来抑制人肺A549细胞的生长。

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