| Background and Purpose:Glutamate-induced excitotoxicity has been implicated in the etiology of ischemic stroke, epilepsy, as well as chronic neurodegenerative disorders, thus, the development of novel neuroprotectant molecules that reduce excitotoxic brain damage is vigorously pursued. Among the glutamate receptor family, the N-methyl-D-aspartate receptor (NMDAR) plays a pivotal role in the process of glutamate-induced excitotoxicity. Accordingly, a significant effort had been made to develop NMDAR antagonists with high-affinity like dizolcipine (MK-801) and phencyclidine previously, although most of these molecules efficiently reduce glutamate neurotoxicity in vitro, their in vivo utility has been heavily questioned due to serious cognitive and psychopathic side effects at clinically effective doses. Thus, the development of novel NMDA receptor with moderate-to-low receptor affinity, and fast on/off blockade kinetics is actively pursued.Ginkgo biloba extract (GBE) has been therapeutically used for several decades to increase peripheral and cerebral blood flow as well as for the treatment of cognitive speed, dementia, and aging damages. Most researchers believed that the extract contains multiple compounds such as flavonoids and terpenoids that contribute to its neuroprotective, but the mechanism still remains elusive. We had ever found GBE could directly and effectively protect cultured neurons against death induced by glutamate compared with MK-801, which indicated GBE could be a good antagonists of NMDAR, in order to elucidate the mechanism, in this study we observe the effects of ginkgo biloba extract (GBE) on NMDA- excitotoxicity in vitro and focal cerebral ischemia in rats, and further explore the...
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