Neuroprotective effects of vanillic acid against oxidative stress induced by cerebral hypoperfusion in male rats

Background and Aim : Free radical-induced neural damage implicated in the pathogenesis of ischemic stroke and antioxidants have protective activity, and neuroprotective strategies investigated to minimize oxidative stress after ischemic events. In the present study, we aimed to investigate the neuroprotective potential of vanillic acid (VA) in an animal model of transient bilateral common carotid artery occlusion and reperfusion (BCCAO/R)Methods : Adult male Wistar rats (250–300 g) randomly divided into four groups and submitted to either cerebral hypoperfusion-reperfusion or a sham surgery after two-weeks of pretreatment with VA and/or normal saline. To induce the animal model of hypoperfusion, bilateral common carotid arteries occluded for 30 min, followed by 72 h of reperfusion. Subsequently, animals decapitated under deep anesthesia and their hippocampi removed for ELISA assaysResults : The results showed that cerebral hypoperfusion significantly increased the level of malondialdehyde (MDA) and decreased enzymatic [glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT)] antioxidant activity in the hippocampus of vehicle- pretreated group as compared to the sham-operated group (p < 0.01, p < 0.01, p < 0.05, and p < 0.01 respectively). While, pretreatment of rats by VA significantly decreased MDA levels and also increased GPx, SOD and CAT enzymatic activity in BCCAO/R rats compared with untreated rats (p < 0.01, p < 0.01, p < 0.05, and p < 0.01 respectively)Conclusion : Our data confirm that VA has antioxidant activity against cerebral hypoperfusion-induced oxidative stress via enhancement of cerebral antioxidant defense, and it can potentially serve as an antioxidant agent against cerebrovascular insufficiency states.

کلیدواژه ها:

Vanillic acid ، Cerebral hypoperfusion ، Oxidative stress ، Rat