Neuroprotective effects of oral gallic acid against oxidative stress induced by 6-hydroxydopamine in rats.

Free radical-induced neural damage is implicated in neurodegenerative diseases and antioxidants have protective activity. In the present study, we examined the effect of gallic acid (GA; 50, 100 and 200mg/kg, p.o. for 10 days) on memory deficit and cerebral oxidative stress induced by 6-hydroxydopamine (6-OHDA; 8 μg/2 μL) injected into the medial forebrain bundle (MFB, full nigral lesion) as an animal model of Parkinson's disease (PD). The results showed that 6-OHDA significantly reduced the passive avoidance memory performance, non-enzymatic (total thiol) and enzymatic [glutathione peroxidase (GPx)] antioxidant contents and increased the level of malondialdehyde (MDA) in the hippocampus and striatum of vehicle-treated group as compared to sham-operated rats. Furthermore, oral administration of GA significantly increased the passive avoidance memory, total thiol and GPx contents and also decreased MDA levels in the above tissues. The results suggest that GA has neuroprotective activity against 6-OHDA-induced oxidative stress via enhancement of cerebral antioxidant defence.