Zinc Oxide Particles Induce Inflammatory Responses in Vascular Endothelial Cells Via Nf-Kappa B Signaling
Resource
JOURNAL OF HAZARDOUS MATERIALS v.183 n.1-3 pp.182-188
Journal
JOURNAL OF HAZARDOUS MATERIALS
Journal Volume
v.183
Journal Issue
n.1-3
Pages
182-188
Date Issued
2010
Date
2010
Author(s)
TSOU, TSUI-CHUN
YEH, SZU-CHING
TSAI, FENG-YUAN
LIN, HO-JANE
CHENG, TSUN-JEN
Abstract
This study investigated inflammatory effects of zinc oxide ( ZnO) particles on vascular endothelial cells. The effects of 50 and 100-nm ZnO particles on human umbilical vein endothelial cells (HUVECs) were characterized by assaying cytotoxicity, cell proliferation, and glutathione levels. A marked drop in survival rate was observed when ZnO concentration was increased to 45 mu g/ml. ZnO concentrations of <= 3 mu g /ml resulted in increased cell proliferation, while those of <= 45 mu g/ml caused dose- dependent increases in oxidized glutathione levels. Treatments with ZnO concentrations <= 45 mu g/ml were performed to determine the expression of intercellular adhesion molecule-1 (ICAM-1) protein, an indicator of vascular endothelium inflammation, revealing that ZnO particles induced a dose-dependent increase in ICAM-1 expression and marked increases in NF-kappa B reporter activity. Overexpression of I kappa B alpha completely inhibited ZnO-induced ICAM-1 expression, suggesting NF-kappa B plays a pivotal role in regulation of ZnO-induced inflammation in HUVECs. Additionally. TNF-alpha, a typical inflammatory cytokine, induced ICAM-1 expression in an NF- kappa B-dependent manner, and ZnO synergistically enhanced TNF-alpha-induced ICAM-1 expression. Both 50 and 100-nm ZnO particles agglomerated to similar size distributions. This study reveals an important role for ZnO in modulating inflammatory responses of vascular endothelial cells via NF- kappa B signaling, which could have important implications for treatments of vascular disease.
Subjects
Zinc oxide
Endothelium
Inflammation
NF-kappa B
Adhesion molecules
Cytokines
SDGs
Type
journal article
