Ginkgo biloba extract (EGb 76 1) has been used therapeutically for centuries. It has attracted great attention as agents for improving circulation, particularly cerebral circulation, which may lead to improved mental function. Many researches hypothesized on the role of the extract in the treatment of diseases involving free radicals and oxidative damage. In the present study, anticonvulsant and antioxidant effects of EGb 761 were investigated in pentylenetetrazol (PTZ)-kindled mice. Valproic acid (VA), a major antiepileptic drug, was also tested for comparison. EGb 761-treated mice displayed a significant attenuated response to PTZ on the test day (day 26) compared with saline-treated and VA-treated animals. Valproic acid significantly increased seizure latency. Pretreatments with EGb 761 significantly protected against PTZ-induced convulsive behaviors (seizure latency, seizure score).
EGb 761 and VA significantly decreased PTZ-induced oxidative injury in brain tissue. EGb 761 was found to be the most effective in preventing PTZ-induced oxidative damage among both substances studied. The data obtained support our speculation that neuroprotective action of EGb 761 may correlate with its ability to inhibit not only excessive reactive oxygen species (ROS) formation but also seizure generation. Taken together, the results of the present study show that the effect of EGb 761 on ROS production contributes to their neuroprotective action. It might be concluded that the suppression of seizure-induced ROS generation may be involved in the mechanism of action of antiepileptic drugs. (c) 2006 Elsevier Inc. All rights reserved.