The effects of gallic acid on pain and memory following transient global ischemia/reperfusion in Wistar rats.

It is generally agreed that most of the phenomena observed during brain ischemia and reperfusion can be explained by the damage to membrane structure. Oxidative stress is resulted in an imbalance between high consumption of oxygen and low levels of endogenous antioxidants. It is known that gallic acid (GA) is a strong antioxidant. The present study was carried out to evaluate the effect of GA on ischemia/reperfusion (I/R)-induced brain injury in rats. Wistar adult male rats weighing 200-250 g were divided into six groups as sham operated (Sh), ischemia/reperfusion (I/R) received normal saline (I+Veh), I/R groups treated with gallic acid (I+GA, 50, 100, or 200 mg/kg, orally, respectively), or with 100 mg /kg phenytoin (I+Phen). The global cerebral I/R injury was induced by occluding bilateral common carotid arteries (BCCA) for 20 min, followed by 5 days reperfusion in adult male rats. It was found that administration of 100 mg/kg GA for 5 days before and 5 days after I/R induction reversed gait performance, sensorimotor disorders (p<0.01), and hypoalgesia (p<0.001) while dose of 50 mg/kg increased passive avoidance memory significantly (p<0.05). Our findings clearly demonstrate that GA has beneficial effects on behavioral impairments after brain injury induced by I/R. The results of this study show that GA pretreatment ameliorates cerebral ischemia/reperfusion injury and enhances the antioxidant defense against BCCA occlusion-induced I/R in rats, so it exhibits cerebroprotective property.