Abstract
The polyphenol resveratrol (RVT) may drive protective mechanisms of cerebral homeostasis during the hypoperfusion/reperfusion triggered by the transient bilateral common carotid artery occlusion followed by reperfusion (BCCAO/R). This immunochemical study investigates if a single dose of RVT modulates the plasticity-related markers brain-derived neurotrophic factor (BDNF), the tyrosine kinase trkB receptor, Polysialylated-Neural Cell Adhesion Molecule (PSA-NCAM), and Activity-regulated cytoskeleton-associated (Arc) protein in the brain cortex after BCCAO/R. Frontal and temporal-occipital cortical regions were examined in male Wistar rats randomly subdivided in two groups, sham-operated and submitted to BCCAO/R. Six hours prior to surgery, half the rats were gavage fed a dose of RVT (180 mg·kg−1 in 300 µL of sunflower oil as the vehicle), while the second half was given the vehicle alone. In the frontal cortex of BCCAO/R vehicle-treated rats, BDNF and PSA-NCAM decreased, while trkB increased. RVT pre-treatment elicited an increment of all examined markers in both sham- and BCCAO/R rats. No variations occurred in the temporal-occipital cortex. The results highlight a role for RVT in modulating neuronal plasticity through the BDNF-trkB system and upregulation of PSA-NCAM and Arc, which may provide both trophic and structural local support in the dynamic changes occurring during the BCCAO/R, and further suggest that dietary supplements such as RVT are effective in preserving the tissue potential to engage plasticity-related events and control the functional response to the hypoperfusion/reperfusion challenge.
Highlights
Emerging evidence indicates that natural products with anti-oxidative and anti-inflammatory properties may prevent and counteract the hypoperfusion/reperfusion tissue challenge induced by acute transient bilateral common carotid artery occlusion followed by reperfusion (BCCAO/R) [1,2,3,4]
ANOVA (Table 1) showed that BCCAO/R-induced molecular changes as well as the effect of the RVT pre-treatment were obvious in the frontal cortex, while no statistically-significant differences were observed in the temporal-occipital cortex
We found that tyrosine kinase receptor B (trkB) underwent BCCAO/R-induced changes opposite to those shown by the brain-derived neurotrophic factor (BDNF), leading to suggest that the trkB and its ligand complement each other to confer resistance and/or reduce brain damage following the hypoperfusion/reperfusion in vehicle-treated rats
Summary
Emerging evidence indicates that natural products with anti-oxidative and anti-inflammatory properties may prevent and counteract the hypoperfusion/reperfusion tissue challenge induced by acute transient bilateral common carotid artery occlusion followed by reperfusion (BCCAO/R) [1,2,3,4]. In the BCCAO/R model, RVT pre-treatment restores the tissue concentration of docosahexaenoic acid (DHA), a structural component of neural cell membranes, and increases expression of synapse-associated proteins [4]. In this context, it is not surprising that RVT has been shown to modulate the expression of brain-derived neurotrophic factor (BDNF) [35,36,37,38], a member of the neurotrophin family that signals through the tyrosine kinase receptor B (trkB). The BDNF-trkB system plays an instructive role for synaptic plasticity [39], involving activation of cytoskeleton dynamics in dendritic spines
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