Electrophysiological, Behavioral and Molecular Study of Vitamin E and Ginkgo biloba in a Rat Model of Alzheimer’s Disease

Abstract

Background and objectives: Alzheimer's disease (AD) is characterized by progressive cognitive decline. Oxidative stress plays a central role in the pathogenesis of AD. It has been proposed that administration of antioxidants affect cognitive processes, such as learning and memory. This study investigated the protective effects of vitamin E and Ginkgo biloba extract (as antioxidants) on learning and memory, hippocampal plasticity, and apoptotic marker proteins in a rat model of AD. Methods: The hyroalcoholic extract of Gingko biloba leaves wasprepared using maceration method. Male Wistar rats were randomly divided into six groups: control, sham received intra-hippocampal injection (I.H.P) of vehicle, AD model that received intra-hippocampal injection of the beta-amyloid (Aβ), AD+ vitamin E (200 mg/kg, i.p.), AD+ G. biloba (100 mg/kg/p.o.), and AD+ vitamin E (200 mg/kg, i.p.)+ G. biloba (100 mg/kg/p.o.). At the end of the treatments, the rats were subjected to the passive avoidance learning (PAL) test. The field long wterm potentials (LTP) were recorded in the hippocampal dentate gyrus. Hippocampal expressions of Bax and Bcl-2 (as pro-apoptotic, as anti-apoptotic) proteins were measured by western blot method. Results: Treatment with G. biloba and vitamin E improved the Aβ-induced memory impairment in the PAL task. Vitamin E and/or G. biloba extract enhanced the population spike amplitude evoked potentials of the LTP components, vitamin E and/or G. biloba extract increased Bcl-2 expression and decreased Bax expression in the hippocampus. Conclusion: Ginkgo biloba and vitamin E could suppress the expression of apoptosis markers and improved hippocampal LTP impairment and the memory deficit induced by Aβ.