Propyl gallate inhibits the growth of calf pulmonary arterial endothelial cells via glutathione depletion

被引:18
作者
Han, Yong Hwan [1 ]
Moon, Hwa Jin [1 ]
You, Bo Ra [1 ]
Park, Woo Hyun [1 ]
机构
[1] Chonbuk Natl Univ, Dept Physiol, Sch Med, Inst Med Sci, Jeonju 561180, South Korea
关键词
Propyl gallate; Apoptosis; Endothelial cells; ROS; GSH; AS4.1 JUXTAGLOMERULAR CELLS; ARSENIC TRIOXIDE; CYCLE ARREST; ANTIOXIDANT ENZYMES; OXIDATIVE STRESS; CALU-6; CELLS; TANNIC-ACID; GALLIC ACID; APOPTOSIS; CYTOTOXICITY;
D O I
10.1016/j.tiv.2010.02.013
中图分类号
R99 [毒物学(毒理学)];
学科分类号
100405 ;
摘要
Propyl gallate (PG) as a synthetic antioxidant exerts a variety of effects on tissue and cell functions. Here, we evaluated the effects of PG on the growth and death of endothelial cells (ECs), especially calf pulmonary artery endothelial cells (CPAEC) in relation to reactive oxygen species (ROS) and glutathione (GSH). PG dose-dependently inhibited the growth of CPAEC and human umbilical vein endothelial cells (HUVEC) at 24 h. PG induced cell death in CPAEC, which was accompanied by the loss of mitochondria] membrane potential (MMP: Delta Psi(m)). PG generally increased ROS level in CPAEC but not in HUVEC. PG also dose-dependently increased GSH depleted cells in both ECs. The treatment with antioxidant of N-acetyl-cysteine (NAC) or ascorbate acid (AA) prevented CPAEC growth inhibition and death by PG, which was accompanied by the attenuation of GSH depletion but not by the reduction of ROS level. In conclusion, PG induced growth inhibition and death of ECs, especially CPAEC via GSH depletion. (C) 2010 Elsevier Ltd. All rights reserved.
引用
收藏
页码:1183 / 1189
页数:7
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