Gallic acid prevents memory deficits and oxidative stress induced by intracerebroventricular injection of streptozotocin in rats

In the present study, we evaluated the effects of gallic acid (GA; 30 mg/kg, orally, once daily for 26 days starting from day 5 prior to streptozotocin injection) on cognitive impairment and cerebral oxidative stress induced by intracerebroventricular-streptozotocin (ICV-STZ; bilaterally, two doses of 3 mg/kg) injection as an animal model of sporadic Alzheimers type (SDAT) in rats. The results showed that ICV-STZ-injection reduced the passive avoidance and spatial memory performance associated with decreased non-enzymatic [total thiol concentration, − 58.5%, − 50.7%] and enzymatic [superoxide dismutase (SOD, − 30.2%, − 32.9%), catalase (CAT, − 43.5%, − 50.7%), glutathione peroxidase (GPx, − 57.1%, − 61.7%)] activities and increased the level of thio-barbituric acid reactive species (TBARS, + 103.5%, + 82.5%) in the hippocampus and cerebral cortex, respectively. In contrast, chronic administration of GA significantly prevented cognitive deficits and biochemical alterations in the ICV-STZ rats. These findings highlight the beneficial role of GA in the ICV-STZ rats via enhancement of cerebral antioxidant defense system. Thus, it may have a therapeutic value for the treatment of SDAT.