t-Resveratrol Protects against Acute High Glucose Damage in Endothelial Cells
Autor: | Raúl Vinet, Marcela Knox, Leda Guzmán, Rocío Álvarez, José L. Martínez, Guillermo Flores, Cristóbal Balada |
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Rok vydání: | 2018 |
Předmět: |
Blood Glucose
Male Nitroprusside 0301 basic medicine Vasodilation 030204 cardiovascular system & hematology Pharmacology Resveratrol Nitric Oxide medicine.disease_cause Umbilical vein Rats Sprague-Dawley 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Stilbenes Human Umbilical Vein Endothelial Cells medicine Animals Humans Endothelial dysfunction Phenylephrine Aorta medicine.disease Acetylcholine Rats Oxidative Stress 030104 developmental biology Postprandial chemistry Cardiovascular Diseases Chemistry (miscellaneous) Hyperglycemia Endothelium Vascular Sodium nitroprusside Reactive Oxygen Species Oxidative stress Food Science medicine.drug |
Zdroj: | Plant Foods for Human Nutrition. 73:235-240 |
ISSN: | 1573-9104 0921-9668 |
Popis: | Postprandial hyperglycemia in diabetic and nondiabetic subjects is associated with endothelial dysfunction. Evidence shows that high glucose generates oxidative stress and a pro-inflammatory state promoting the development of cardiovascular diseases. trans-Resveratrol (t-RV) has been shown to reduce cardiovascular risk. To determine whether t-RV acts as a protector against acute high glucose (AHG)-induced damage, two in vitro models, rat aortic rings (RAR) and human umbilical vein endothelial cells (HUVEC) were used. RAR pretreated with AHG (25 mM D-glucose) for 3 h dramatically decreased the endothelium-dependent relaxation (EDR) induced by acetylcholine in phenylephrine (PE)-precontracted vessels. However, coincubation with t-RV significantly mitigated the damage induced by AHG on EDR. Pretreatment with AHG did not affect the vasodilation induced by sodium nitroprusside. HUVEC treated with t-RV decreased cytotoxicity and reduced radical oxygen species production induced by AHG. Taken together, these results suggest that t-RV can mitigate the AHG-induced EDR damage through a mechanism involving ROS scavenging and probably an increase in the bioavailability of NO. |
Databáze: | OpenAIRE |
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