Abstract
The reactive oxygen species (ROS) are known to play a major role in many pathophysiological conditions, such as ischemia and reperfusion injury. The present study was aimed to evaluate the in vivo cyanidin (anthocyanin) effects on damages induced by rat pial microvascular hypoperfusion-reperfusion injury by cerebral blood flow decrease (CBFD) and subsequent cerebral blood flow recovery (CBFR). In particular, the main purpose was to detect changes in ROS production after cyanidin administration. Rat pial microvasculature was investigated using fluorescence microscopy through a cranial window (closed); Strahler's method was utilized to define the geometric features of pial vessels. ROS production was investigated in vivo by 2′-7′-dichlorofluorescein-diacetate assay and neuronal damage was measured on isolated brain sections by 2,3,5-triphenyltetrazolium chloride staining. After 30 min of CBFD, induced by bilateral common carotid artery occlusion, and 60 min of CBFR, rats showed decrease of arteriolar diameter and capillary perfusion; furthermore, increase in microvascular leakage and leukocyte adhesion was observed. Conversely, cyanidin administration induced dose-related arteriolar dilation, reduction in microvascular permeability as well as leukocyte adhesion when compared to animals subjected to restriction of cerebral blood flow; moreover, capillary perfusion was protected. ROS generation increase and marked neuronal damage were detected in animals subjected to CBFD and CBFR. On the other hand, cyanidin was able to reduce ROS generation and neuronal damage. In conclusion, cyanidin treatment showed dose-related protective effects on rat pial microcirculation during CBFD and subsequent CBFR, inducing arteriolar dilation by nitric oxide release and inhibiting ROS formation, consequently preserving the blood brain barrier integrity.
Highlights
Many evidences indicate that a diet rich in antioxidants is associate to a decreased incidence of cardiovascular diseases, such as stroke, acute myocardial disease or cancer (Galvano et al, 2004; Lapi et al, 2016)
The aim of this study was to investigate the in vivo effects of cyanidin on oxidative stress and changes in rat pial microvasculature determined by 30 min of cerebral blood flow decrease (CBFD) and 60 min of cerebral blood flow recovery (CBFR)
The present data indicate that cyanidin, a polyphenol widely diffused in nature, was able to counteract oxidative stress and microvascular changes induced by 30 min of cerebral blood flow decrease, caused by bilateral occlusion of common carotid arteries, and 60 min of cerebral blood flow recovery
Summary
Many evidences indicate that a diet rich in antioxidants is associate to a decreased incidence of cardiovascular diseases, such as stroke, acute myocardial disease or cancer (Galvano et al, 2004; Lapi et al, 2016). Anthocyanins, belonging to polyphenol family, are one of the natural antioxidants responsible of fruit and flower colors (red, orange and blue) and play an important role in counteracting the oxidative stress induced by reactive oxygen species (ROS). These radicals have been related to different pathophysiological conditions (Serraino et al, 2003; Accetta et al, 2016; Mondola et al, 2016). The protective role of natural anthocyanins has been demonstrated to be effective against ischemia/reperfusion injury in different organs, such as kidney, heart and intestine (Jakesevic et al, 2013; Quintieri et al, 2013; Isaak et al, 2017). After 2, 4, and 6 months of oral supplementation, anthocyanins were able to counteract microvascular changes such as arteriolar vasoconstriction, increase of microvascular permeability and leukocyte adhesion (Mastantuono et al, 2016)
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