Myricetin preserves rat pial microcirculation from injury induced by cerebral hypoperfusion and reperfusion

Abstract

Background/Objective: Myricetin, a flavonoid compound, is widely diffused in vegetables, fruits and beverages, well known for its antioxidant and anti-inflammatory properties. The present study was aimed to investigate the acute effects of myricetin on the pial microvascular alterations and oxygen-derived free radical formation, due to 30 min cerebral blood flow lowering (CBFL) and subsequent cerebral blood flow resumption (CBFR). Methods: Rat pial microvasculature was investigated using fluorescence microscopy through a closed cranial window. At first, arterioles were classified according to the Strahler’s ordering scheme. Then, arteriolar diameter, permeability increase, leukocyte adhesion to venular walls, perfused capillary length (CPL) and red blood cell velocity (VRBC) were quantified by computerized methods. Finally, reactive oxygen species (ROS) production was investigated in vivo by 2 ′ -7 ′ -dichlorofluorescein- diacetate assay and infarct size by 2,3,5-triphenyltetrazolium chloride staining. Results: After 30 min CBFL and 60 min CBFR, a decrease of arteriolar diameter, CPL and VRBC was detected; furthermore, increases in microvascular leakage and leukocyte adhesion were observed in hypoperfused animals. Conversely, myricetin administration induced dose-related arteriolar dilation, reduction in microvascular permeability as well as leukocyte adhesion when compared to those detected in bilateral common carotid artery occlusion-submitted animals; moreover, CPL and VRBC were preserved. In animals treated with myricetin the ROS production was blunted and infarct size significantly reduced. Conclusion: In conclusion, myricetin acute administration showed dose-related protective effects on rat pial microcirculation during CBFL and subsequent CBFR, inducing arteriolar dilation and inhibiting ROS formation, consequently preserving the blood brain barrier integrity.