Abstract
Methods: Thirty-two adult male Wistar rats (220±20g). The rats were divided randomly into four groups of 8 in each: 1) Sham+Veh; 2) Sham+GSE; 3) Isch+Veh; 4) Isch+GSE. In order to make animal model of permanent cerebral hypoperfusion/ischemia, both carotid arteries were ligated upper and lower and cut bilaterally. The animals in the treatment groups received a dose of 100 mg/kg GSE daily, by oral gavage (PO) for 4 weeks. Malondialdehyde (MDA) levels, Glutathione peroxidase (GPx) activity, and total thiol (–SH) groups were measured in homogenate of cerebral hippocampus and cortex.
Results: MDA elevated significantly in rats’ hippocampus and cortex after chronic cerebral hypoperfusion/ischemia when compared with sham rats (P<0.05 and P<0.001 respectively). Biochemical examinations revealed that GSE reversed the increased level of brain tissue malondialdehyde (MDA), and attenuated decreased activity of glutathione peroxidase (GPx) in BCCAO rats.
Conclusion: These findings suggest that GSE exhibits therapeutic potential for oxidative stress induced by cerebral hypoperfusion/ischemia, which is most likely related, at least in part, to its antioxidative and free radical scavenging actions.