Department of Physiology, Medical School, Centers for Healthcare Technology Development Institute for Medical Sciences Chonbuk National University, Jeonju, Republic of Korea.
Oncol Rep. 2010 Jan;23(1):287-92.
Pyrogallol (PG) as a polyphenol compound induces apoptosis in several types of cells. Here, we evaluated the effects of PG on endothelial cells (ECs), especially calf pulmonary artery endothelial cells (CPAEC) in relation to the cell growth, ROS and glutathione (GSH) levels. PG dose-dependently inhibited the growth of CPAEC and human umbilical vein endothelial cells (HUVEC) at 24 h. PG also induced apoptosis in CPAEC, which was accompanied by the loss of mitochondrial membrane potential (MMP; DeltaPsim). PG decreased ROS level including O2*- and PG dose-dependently increased GSH depleted cell number in both EC types. N-acetyl-cysteine (NAC; a well-known antioxidant) increased ROS levels in PG-treated CPAEC with the prevention of cell death and GSH depletion. In conclusion, PG inhibited the growth of ECs, especially CPAEC via apoptosis. PG-induced EC death was related to GSH depletion rather than ROS level changes.
焦性没食子酸（PG）作为一种多酚化合物，能诱导多种类型的细胞凋亡。在这里，我们评估了 PG 对内皮细胞（ECs）的影响，特别是小牛肺动脉内皮细胞（CPAEC），涉及细胞生长、ROS 和谷胱甘肽（GSH）水平。PG 呈剂量依赖性地在 24 小时内抑制 CPAEC 和人脐静脉内皮细胞（HUVEC）的生长。PG 还诱导 CPAEC 凋亡，伴随线粒体膜电位（MMP；DeltaPsim）的丧失。PG 降低 ROS 水平，包括 O2*-，并呈剂量依赖性地增加两种 EC 类型中 GSH 耗竭细胞的数量。N-乙酰半胱氨酸（NAC；一种众所周知的抗氧化剂）增加了 PG 处理的 CPAEC 中的 ROS 水平，同时预防了细胞死亡和 GSH 耗竭。总之，PG 通过凋亡抑制 ECs 的生长，特别是 CPAEC。PG 诱导的 EC 死亡与 GSH 耗竭有关，而不是 ROS 水平的变化。
