Ginkgo biloba leaf extract improves the cognitive abilities of rats with D-galactose induced dementia

Department of Neurology, the First People's Hospital, Xuzhou, Jiangsu 221002, China
Journal of biomedical research 01/2013; 27(1):29-36. DOI: 10.7555/JBR.27.20120047
Source: PubMed


Standardized Ginkgo biloba leaf extract has been used in clinical trials for its beneficial effects on brain functions, particularly in dementia. Substantial experimental evidences indicated that Ginkgo biloba leaf extract (EGB) protected neuronal cells from a variety of insults. We investigated the effect of EGB on cognitive ability and protein kinase B (PKB) activity in hippocampal neuronal cells of dementia model rats. Rats received an intraperitoneal injection of D-galactose to induce dementia. Forty-eight Spraque-Dawley rats were randomly divided into six groups, including the control group, D-galactose group (Gal), low-dose EGB group (EGB-L), mid-dose EGB group (EGB-M), high-dose EGB group (EGB-H) and treatment group. The EGB-L, EGB-M and EGB-H groups were administered with EGB and D-galactose simultaneously. Y-maze, cresyl violet staining, TUNEL assays and immunohistochemistry staining were performed to detect learning and memory abilities, morphological changes in the hippocampus, neuronal apoptosis and the expressing level of phospho-PKB, respectively. Rats in the Gal group showed decreased abilities of learning and memory, and hippocampal pyramidal cell layer was damaged, while EGB administration improved learning and memory abilities. The Gal group exhibited many stained, condensed nuclei and micronuclei, either isolated or within the cytoplasm of cells (39.5±1.4). Apoptotic cells decreased in the groups of EGB-L (35.9±0.9), EGB-M (16.8±1.0) and EGB-H (10.1±0.8), and there were statistical significances compared with the Gal group. Immunoreactivity of phospho-PKB was localized diffusely throughout the cytosol of cells in all groups, while the immunoreactivity of the Gal group was weak. EGB significantly attenuated learning and memory impairment in a dose-dependent manner, while it could decrease the nmber of TUNEL-positive cells, and increase the activity of PKB. Our results demonstrated that EGB attenuated memory impairment and cell apoptosis in galactose-induced dementia model rats by activating PKB.

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Available from: Deqin Geng, Jan 14, 2014
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    • "In order to understand the mechanisms that occur during the aging process in the brain and the pathological lapse in neurodegeneration of these mechanisms, we aimed to discover in vivo biomarkers for these processes through appropriate animal models. Several contributions have reported that long-term systemic administration of d-gal to rats causes neurodegeneration, induces changes that resemble natural aging in animals, including deterioration of cognitive and motor skills, a shortened lifespan, and oxidative stress [4] [5] [6] [7]. d-gal is a normal substance in the body. "
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    ABSTRACT: The aim of study was to search for new biomarkers with a magnetic resonance technique to identify the early stages of dementia, induced by D-galactose, and evaluate Simvastatin therapy. Localized proton magnetic resonance spectroscopy measurements showed a significant decrease in the concentration of N-acetylaspartate+N-acetylaspartylglutamate and myo-inositol in the D-galactose group compared to the control group, and, conversely, an increase of N-acetylaspartate+N-acetylaspartylglutamate in the D-galactose/Simvastatin group. Using a saturation transfer experiment, with phosphorus magnetic resonance spectroscopy, we observed a significant elevation of the forward rate constant of the creatine kinase reaction in the brains of the D-galactose group compared to controls, and subsequently, a significant reduction of this reaction in the D-galactose/Simvastatin group. Spatial learning and memory were evaluated using the modified Morris water maze test. The dynamics of the learning process represented by the learning index revealed a significant reduction in learning in the D-galactose group, but the deficits as a consequence of the D-galactose effects were recovered in the D-galactose/Simvastatin group, in which the learning dynamics resembled those of the control group. By determining the thiobarbituric acid reactive substances and total coenzyme Q9 in plasma, we have shown that long-term administration of D-galactose created conditions for oxidative stress, and that the administration of Simvastatin decreased oxidative stress in plasma. Volumetry analyses from the hippocampal area show a reduction in the segmented area in the D-galactose group, compared with the control group, and an enlarged area in the hippocampus in the D-galactose/Simvastatin group. Copyright © 2015. Published by Elsevier B.V.
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    • "Modern pharmacological studies revealed that Ginkgo biloba possessed neuroprotective effects towards D-galactose [15], beta-amyloid [16], and ischemia-induced neuronal death [17]. Uncaria rhynchophylla also prevented D-galactose [18], beta-amyloid [19], 6-hydroxydopamine [20], and kainic acidinduced neurotoxicity [21]. "
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