Suppressive effects of quercetin on hydrogen peroxide-induced caveolin-1 phosphorylation in endothelial cells

  • Kondo-Kawai Akari
    Department of Food Science, Graduate School of Biomedical Sciences, Tokushima University Department of Public Health and Applied Nutrition, Institute of Biomedical Sciences, Tokushima University Graduate School Laboratory of Nutritional Science, Shikoku Junior College
  • Sakai Tohru
    Department of Public Health and Applied Nutrition, Institute of Biomedical Sciences, Tokushima University Graduate School
  • Terao Junji
    Department of Food Science, Graduate School of Biomedical Sciences, Tokushima University Faculty of Clinical Nutrition and Dietetics, Konan Women’s University
  • Mukai Rie
    Department of Food Science, Graduate School of Biomedical Sciences, Tokushima University Department of Food Science, Graduate School of Technology, Industrial ‍and ‍Social Sciences, Tokushima University

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<p>Caveolin-1 is a major protein of the caveolae structure in vascular endothelial cell membrane. Phosphorylation of caveolin-1 is one of the initial events leading to exacerbation of vascular permeability caused by oxidative stress. Although quercetin is known to be an anti-atherosclerosis factor that acts as a dietary antioxidant, little is known about its role in the regulation of caveolin-1 phosphorylation. In this study, we investigated the inhibitory effect of quercetin on hydrogen peroxide-induced caveolin-1 phosphorylation in human umbilical vein endothelial cells. Quercetin inhibited caveolin-1 phosphorylation in cells pretreated with quercetin for 24 h and then exposed to hydrogen peroxide. However, quercetin 3-O-β-glucuronide, a conjugated metabolite of quercetin, did not exert this inhibitory effect. Exposure to hydrogen peroxide increased vascular permeability and reduced mRNA expression of the intercellular adhesion protein, vascular endothelial cadherin (VE-cadherin). By contrast, pretreatment with quercetin suppressed the increase in vascular permeability and decreased VE-cadherin expression. These results indicate that deconjugated quercetin can play a role in the prevention of altered vascular permeability under oxidative stress by suppressing caveolin-1 phosphorylation. Thus, dietary quercetin may be beneficial for the maintenance of endothelial cell function.</p>

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