Premium
Co‐enzyme Q10 mitigate oxidized LDL‐induced endothelial inflammation: Role of ROS and NF‐κB signaling
Author(s) -
Wu YunJhen,
Tsai KunLing,
Ou HsiuChung
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.1038.4
Subject(s) - coenzyme q10 , inflammation , chemistry , umbilical vein , human umbilical vein endothelial cell , p38 mitogen activated protein kinases , antioxidant , pharmacology , nf κb , cell adhesion molecule , reactive oxygen species , microbiology and biotechnology , signal transduction , biochemistry , mapk/erk pathway , medicine , immunology , biology , in vitro
Oxidized low‐density lipoprotein (oxLDL) plays a key role in the generation and progression of atherosclerosis, which is considered as a chronic inflammatory disease. Coenzyme Q10 (CoQ) has long been utilized as a cardioprotective agent in various heart diseases. One of the most important mechanisms by which CoQ exerts cardioprotection is aerobic ATP production as a mobile electron carrier in the mitochondrial electron transfer chain. The ability of CoQ to afford myocardial protection is also attributed to its antioxidant property. The aim of this study was to examine whether CoQ could prevent oxLDL‐induced endothelial inflammation and to explore the potential mechanisms. Primary human umbilical vein endothelial cell cultures (HUVECs) were incubated with CoQ for 2 hours followed by incubated with oxLDL for additional 24 hours. We found that oxLDL‐induced ROS generation, p38 MAPK phosphorylation subsequent activation of nuclear factor κB (NF‐κB) and up‐regulated relative down stream inflammatory cytokines and adhesion molecules and the adherence of monocytic THP‐1 cells to HUVECs. These detrimental effects were ameliorated dose dependently by CoQ (P<0.05). Results from this study may provide insight into a possible molecular mechanism underlying CoQ suppression of the oxLDL‐mediated in endothelial inflammation.