期刊
FOOD AND CHEMICAL TOXICOLOGY
卷 48, 期 5, 页码 1334-1340出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.fct.2010.02.034
关键词
Gallic acid; Apoptosis; Caspase; ROS; GSH
资金
- Ministry for Health, Welfare & Family Affairs and Republic of Korea [A084194]
Gallic acid (GA) is widely distributed in various plants and foods, and its various biological effects have been reported. Here, we evaluated the effects of GA on HeLa cells in relation to cell growth inhibition and death. HeLa cell growth was diminished with an IC50 of approximately 80 mu M GA at 24 h whereas an IC50 of GA in human umbilical vein endothelial cells (HUVEC) was approximately 400 mu M. GA-induced apoptosis and/or necrosis in HeLa cells and HUVEC, which was accompanied by the loss of mitochondrial membrane potential (MMP; Delta Psi(m)). The percents of MMP (Delta Psi(m)) loss cells and death cells were lower in HUVEC than HeLa cells. All the tested caspase inhibitors (pan-caspase, caspase-3, -8 or -9 inhibitor) significantly rescued HeLa cells from GA-induced cell death. GA increased reactive oxygen species (ROS) level and GSH (glutathione) depleted cell number in HeLa cells. Caspase inhibitors reduced GSH depleted cell number but not ROS level in GA-treated HeLa cells. In conclusion, GA inhibited the growth of HeLa cells and HUVEC via apoptosis and/or necrosis. The susceptibility of HeLa cells to GA was higher than that of HUVEC. GA-induced HeLa cell death was accompanied by ROS increase and GSH depletion. (C) 2010 Elsevier Ltd. All rights reserved.
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