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.
    Full-text · Article · Feb 2015 · Behavioural Brain Research
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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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    ABSTRACT: This study aims to investigate the neuroprotective effect of the rhizome of Gastrodia elata (GE) aqueous extract on beta-amyloid(A β )-induced toxicity in vivo and in vitro. Transgenic Drosophila mutants with A β -induced neurodegeneration in pan-neuron and ommatidia were used to determine the efficacy of GE. The antiapoptotic and antioxidative mechanisms of GE were also studied in A β -treated pheochromocytoma (PC12) cells. In vivo studies demonstrated that GE (5 mg/g Drosophila media)-treated Drosophila possessed a longer lifespan, better locomotor function, and less-degenerated ommatidia when compared with the A β -expressing control (all P < 0.05). In vitro studies illustrated that GE increased the cell viability of A β -treated PC12 cells in dose-dependent manner, probably through attenuation of A β -induced oxidative and apoptotic stress. GE also significantly upregulated the enzymatic activities of catalase, superoxide dismutase, and glutathione peroxidase, leading to the decrease of reactive oxidation species production and apoptotic marker caspase-3 activity. In conclusion, our current data presented the first evidence that the aqueous extract of GE was capable of reducing the A β -induced neurodegeneration in Drosophila, possibly through inhibition of apoptosis and reduction of oxidative stress. GE aqueous extract could be developed as a promising herbal agent for neuroprotection and novel adjuvant therapies for Alzheimer's disease.
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    ABSTRACT: Gingko biloba extract (EGB) has been used in traditional medicines for centuries, and although its application to cerebral ischemia has been of great interest in recent years, high quality evidence-based clinical trials have not been carried out. This systematic review and meta-analysis aimed to examine the neuroprotective effect of EGB on focal cerebral ischemia in animal models. A systematic literature search was performed using five databases spanning January 1980-July 2013. The outcome was assessed using the effect size, which was based on infarct size and/or neurological score. A total of 42 studies with 1,232 experimental animals matched our inclusion criteria. The results revealed that EGB improved the effect size by 34% compared to the control group. The animal species, the method and time to measure outcome, and the route and dosage of EGB administration affected the variability of the effect size. Mechanisms of EGB neuroprotection were reported as anti-apoptotic, anti-oxidative, and anti-inflammatory. In conclusion, EGB exerts a significant protective effect on experimental focal cerebral ischemia. However, possible experimental bias should be taken into account in future clinical studies.
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