Effect of Vitamin E and Omega-3 Fatty Acids on Protecting Ambient PM2.5-Induced Inflammatory Response and Oxidative Stress in Vascular Endothelial Cells

• Published in: PloS one Vol. 11; no. 3; p. e0152216
• Main Authors: Bo, Liang, Jiang, Shuo, Xie, Yuquan, Kan, Haidong, Song, Weimin, Zhao, Jinzhuo
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 23.03.2016; Public Library of Science (PLoS)
• Subjects: Air pollution; Antioxidants; Biology and Life Sciences; Biomarkers; Cardiology; Cytokines; Cytokines - metabolism; Cytokines - physiology; Cytoplasm; Disease; Drug dosages; Endothelial cells; Endothelial Cells - drug effects; Endothelial Cells - metabolism; Endothelial Cells - physiology; Environmental health; Fatty acids; Fatty Acids, Omega-3 - pharmacology; Human Umbilical Vein Endothelial Cells - drug effects; Human Umbilical Vein Endothelial Cells - metabolism; Human Umbilical Vein Endothelial Cells - physiology; Humans; Inflammation; Inflammation - chemically induced; Inflammation - prevention & control; Inflammatory response; Injuries; Interleukin 6; Laboratories; Malondialdehyde; Malondialdehyde - metabolism; Medical research; Medicine and Health Sciences; Nutrients; Outdoor air quality; Oxidative stress; Oxidative Stress - drug effects; Oxygen; Particulate matter; Particulate Matter - adverse effects; Permeability; Pollutants; Public health; Reactive oxygen species; Reactive Oxygen Species - metabolism; Rodents; Studies; Superoxide dismutase; Superoxide Dismutase - metabolism; Tocopherol; Tumor necrosis factor-TNF; Tumor necrosis factor-α; Umbilical vein; Vitamin E; Vitamin E - pharmacology; China
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0152216

Although the mechanisms linking cardiopulmonary diseases to ambient fine particles (PM2.5) are still unclear, inflammation and oxidative stress play important roles in PM2.5-induced injury. It is well known that inflammation and oxidative stress could be restricted by vitamin E (Ve) or omega-3 fatty acids (Ω-3 FA) consumption. This study investigated the effects of Ve and Ω-3 FA on PM2.5-induced inflammation and oxidative stress in vascular endothelial cells. The underlying mechanisms linking PM2.5 to vascular endothelial injury were also explored. Human umbilical vein endothelial cells (HUVECs) were treated with 50 μg/mL PM2.5 in the presence or absence of different concentrations of Ve and Ω-3 FA. The inflammatory cytokines and oxidative stress markers were determined. The results showed that Ve induced a significant decrease in PM2.5-induced inflammation and oxidative stress. Malondialdehyde (MDA) in supernatant and reactive oxygen species (ROS) in cytoplasm decreased by Ve, while the superoxide dismutase (SOD) activity elevated. The inflammatory cytokines interleukin 6 (IL-6) and tumor necrosis factor α (TNF-α) also reduced by Ve. Moreover, Ω-3 FA played the same role on decreasing the inflammation and oxidative stress. IL-6 and TNF-α expressions were significantly lower in combined Ve with Ω-3 FA than treatment with Ve or Ω-3 FA alone. The Ve and Ω-3 FA intervention might abolish the PM2.5-induced oxidative stress and inflammation in vascular endothelial cells. There might be an additive effect of these two nutrients in mediating the PM2.5-induced injury in vascular endothelial cells. The results suggested that inflammation and oxidative stress might be parts of the mechanisms linking PM2.5 to vascular endothelial injury.