Coenzyme Q10 Prevents Senescence and Dysfunction Caused by Oxidative Stress in Vascular Endothelial Cells

Oxidative damage in endothelial cells is proposed to play an important role in endothelial dysfunction and atherogenesis. We previously reported that the reduced form of coenzyme Q10 (CoQ(10)H(2)) effectively inhibits oxidative stress and decelerates senescence in senescence-accelerated mice. Here, we treated human umbilical vein endothelial cells (HUVECs) with H(2)O(2) and investigated the protective effect of CoQ(10)H(2) against senescence, oxidative damage, and reduction in cellular functions. We found that CoQ(10)H(2) markedly reduced the number of senescence-associated β-galactosidase-positive cells and suppressed the expression of senescence-associated secretory phenotype-associated genes in H(2)O(2)-treated HUVECs. Furthermore, CoQ(10)H(2) suppressed the generation of intracellular reactive oxygen species (ROS) but promoted NO production that was accompanied by increased eNOS expression. CoQ(10)H(2) prevented apoptosis and reductions in mitochondrial function and reduced migration and tube formation activity of H(2)O(2)-treated cells. The present study indicated that CoQ(10)H(2) protects endothelial cells against senescence by promoting mitochondrial function and thus could delay vascular aging.