Vanillic acid attenuates effects of transient bilateral common carotid occlusion and reperfusion in rats

Cerebral hypoperfusion induced by transient bilateral common carotid arteries occlusion (tBCCAO), is associated with deleterious alterations in several physiological parameters of the animals. This study aims to investigate the effects of vanillic acid (VA) on memory impairment, locomotion and exploratory deficits, as well as histological and hippocampal long-term potentiation (LTP) injuries induced by tBCCAO procedure followed by reperfusion (BCCAO/R) in rats. Adult male Wistar rats (250-300 g) were divided randomly into four groups: Sham-Operated group “Sham”; Vehicle + BCCAO/R group “BCCAO/R”; Vehicle+ Vanillic acid group “VA”; VA (100 mg/kg) +BCCAO/R group “VA +BCCAO/R”. Cerebral hypoperfusion was induced after 14 days of pretreatment with VA and/or normal saline. To induce the animal model of hypoperfusion, bilateral common carotid arteries were occluded for 30 min, followed by 72 h of reperfusion. Subsequently, behavioral, histopathological and electrophysiological parameters were evaluated after BCCAO/R. Data showed that pretreatment of VA markedly improved locomotion in tBCCAO rats compared with the untreated BCCAO/R rats (p < 0.05). Moreover, pretreatment of VA significantly ameliorated memory impairment in “VA + BCCAO/R” group compared with the “BCCAO/R” group (P < 0.01). The field excitatory postsynaptic potential (fEPSP) amplitude and slope were significantly decreased in “BCCAO/R” group compared with Sham group (P < 0.001). Data indicate that fEPSP amplitude and slope were increased in “VA + BCCAO/R” group compared with the “BCCAO/R” group (P < 0.001). Furthermore, histopathological observation in VA pretreated tBCCAO rats showing markedly attenuated of cell death (P < 0.01) and arrangement of CA1 neurons as compared with the untreated BCCAO/R rats. Our data confirm the protective role of VA against transient cerebral ischemia and reperfusion in rats. Moreover, it proposes that VA has a beneficial role in cerebrovascular insufficiency states.