Protective Effects of N-Acetyl Cysteine against Diesel Exhaust Particles-Induced Intracellular ROS Generates Pro-Inflammatory Cytokines to Mediate the Vascular Permeability of Capillary-Like Endothelial Tubes.

摘要: Exposure to diesel exhaust particles (DEP) is associated with pulmonary and cardiovascular diseases. Previous studies using in vitro endothelial tubes as a simplified model of capillaries have found that DEP-induced ROS increase vascular permeability rearrangement or internalization adherens junctional VE-cadherin away from the plasma membrane. This allows DEPs penetrate into cell capillary lumen. In addition, pro-inflammatory cytokines are up-regulated mediate response DEP. However, mechanisms through which these remain unknown. Hence, we examined ability DEP induce human umbilical vein tube cells investigate mechanisms. Furthermore, supplementation NAC reduces production following exposure HUVEC contributed intracellular generation. Endothelial oxidative stress induced release TNF-α IL-6 cells, subsequently stimulating secretion VEGF-A independent HO-1. Our data suggests TNF- α IL-6, would contribute disrupt cell-cell borders vasculature permeability. Addition suppresses efficiently subsequent damages by increasing endogenous glutathione.