t-Resveratrol Protects against Acute High Glucose Damage in Endothelial Cells
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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.
KeywordsPostprandial hyperglycemia Acute high glucose Oxidative stress Rat aorta Human umbilical vein endothelial cells Resveratrol
Acute high glucose
The concentration of the compound that gives half-maximal response
Emax maximal effect (relaxation)
Human umbilical vein endothelial cells
Rat aortic rings
Reactive oxygen species
This work was supported by Grants DIUV No. 57/2011 from Universidad de Valparaíso, Chile; Grant CREAS No. R12C1001 from CONICYT-REGIONAL, GORE Región de Valparaíso, Chile; Grant No. 037-274 from Pontificia Universidad Católica de Valparaíso, Chile and Grant DICYT-USACH No. 021643MS from JLM.
Compliance with Ethical Standards
Conflicts of Interest
The authors state no conflict of interest.
- 9.Tesfamariam B, Brown ML, Cohen RA (1992) Aldose reductase and myo-inositol in endothelial cell dysfunction caused by elevated glucose. J Pharmacol Exp Ther 263:153–157Google Scholar
- 20.Wu D, Yotnda P (2011) Production and detection of reactive oxygen species (ROS) in cancers. J Vis Exp 57:e3357Google Scholar
- 23.Min Z, Kang L, Lin L et al (2010) Resveratrol restores lysophosphatidylcholine-induced loss of endothelium-dependent relaxation in rat aorta tissue coinciding with inhibition of extracellular-signal-regulated protein kinase activation. Phytother Res 24:1762–1768Google Scholar
- 27.Mokhtar SS, Rasool AH (2015) Role of endothelium-dependent hyperpolarisation and prostacyclin in diabetes. Malays J Med Sci 22:8–17Google Scholar