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.
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Huo et al. (2018) studied this question.