Ferulic acid-4-O-sulfate rather than ferulic acid relaxes arteries and lowers blood pressure in mice |
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| Affiliation: | 1. Department of Food Safety and Food Quality, Faculty of Bioscience Engineering, Ghent University, Coupure Links 653, 9000 Gent, Belgium;2. Department of Pharmacology, Faculty of Medicine and Health Sciences, Ghent University, De Pintelaan 185, 9000 Gent, Belgium;3. Department of Biomedical Molecular Biology, Faculty of Sciences, Ghent University-VIB, Technologiepark 927, 9052 Gent, Belgium;4. Department of Crop Protection, Faculty of Bioscience Engineering, Ghent University, Coupure Links 653, 9000 Gent, Belgium;5. School of Food Science and Nutrition, University of Leeds, Leeds LS2 9JT, UK;1. Luxembourg Institute of Health (L.I.H.) (formerly CRP-Santé), Centre d''Etudes en Santé, Strassen, Grand Duchy of Luxembourg;2. Nutritional Physiology Research Centre, University of South Australia, Adelaide, Australia;3. Department of Psychology, University of Maine, Orono, ME, USA;4. Graduate School of Biomedical Science and Engineering, University of Maine, Orono, ME, USA;1. Health Care Food Research Laboratories, Kao Corporation, Tokyo 131-8501, Japan;2. Department of Laboratory and Vascular Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima City, 890-8520, Japan |
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| Abstract: | Consumption of foods rich in ferulic acid (FA) such as wholegrain cereals, or FA precursors such as chlorogenic acids in coffee, is inversely correlated with risk of cardiovascular disease and type 2 diabetes. As a result of digestion and phase II metabolism in the gut and liver, FA is converted predominantly into ferulic acid-4-O-sulfate (FA-sul), an abundant plasma metabolite. Although FA-sul is the main metabolite, very little has been reported regarding its bioactivities. We have compared the ex vivo vasorelaxing effect of FA and FA-sul (10−7–3.10−5 M) on isolated mouse arteries mounted in tissue myographs. FA-sul, but not FA, elicited a concentration-dependent vasorelaxation of saphenous and femoral arteries and aortae. The FA-sul-mediated vasorelaxation was blunted by 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one, a soluble guanylate cyclase (sGC) inhibitor. The role of sGC was confirmed in femoral arteries isolated from sGCα1(−/−) knockout mice. Furthermore, 4-aminopyridine, a specific inhibitor of voltage-dependent potassium channels, significantly decreased FA-sul-mediated effects. In anesthetized mice, intravenous injection of FA-sul decreased mean arterial pressure, whereas FA had no effect, confirming the results obtained ex vivo. FA-sul is probably one of the major metabolites accounting for the blood pressure-lowering effects associated with FA consumption. |
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