Hydrogen sulfide: A novel mechanism for the vascular protection by resveratrol under oxidative stress in mouse aorta
| Autor: | Asif Ahmed, Gulnur Sevin, Mehmet Vehbi Dereli, Gunay Yetik-Anacak, Ozge Ozzayim |
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| Rok vydání: | 2016 |
| Předmět: |
Male
0301 basic medicine Antioxidant Physiology medicine.medical_treatment Endogeny Vasodilation Pyrogallol Resveratrol Nitric Oxide medicine.disease_cause Antioxidants Nitric oxide Mice 03 medical and health sciences chemistry.chemical_compound Stilbenes medicine Animals Cysteine Hydrogen Sulfide Aorta Pharmacology chemistry.chemical_classification Reactive oxygen species equipment and supplies Oxidative Stress 030104 developmental biology chemistry Biochemistry Biophysics Molecular Medicine Reactive Oxygen Species Oxidative stress |
| Zdroj: | Vascular Pharmacology. 87:76-82 |
| ISSN: | 1537-1891 1879-3649 |
| Popis: | Reactive oxygen species (ROS) decreases bioavailability of nitric oxide (NO) and impairs NO-dependent relaxations. Like NO, hydrogen sulfide (H2S) is an antioxidant and vasodilator; however, the effect of ROS on H2S-induced relaxations is unknown. Here we investigated whether ROS altered the effect of H2S on vascular tone in mouse aorta and determined whether resveratrol (RVT) protects it via H2S. Pyrogallol induced ROS formation. It also decreased H2S formation and relaxation induced by L-cysteine and in mouse aorta. Pyrogallol did not alter sodium hydrogensulfide (NaHS)-induced relaxation suggesting that the pyrogallol effect on L-cysteine relaxations was due to endogenous H2S formation. RVT inhibited ROS formation, enhanced L-cysteine-induced relaxations and increased H2S level in aortas exposed to pyrogallol suggesting that RVT protects against "H2S-dysfunctions" by inducing H2S formation. Indeed, H2S synthesis inhibitor AOAA inhibited the protective effects of RVT. RVT had no effect on Ach-induced relaxation that is NO dependent and the stimulatory effect of RVT on H2S-dependent relaxation was also independent of NO. These results demonstrate that oxidative stress impairs endogenous H2S-induced relaxations and RVT offers protection by inducing H2S suggesting that targeting endogenous H2S pathway may prevent vascular dysfunctions associated by oxidative stress. (C) 2016 Published by Elsevier Inc. |
| Databáze: | OpenAIRE |
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