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      Total flavonoids of Selaginella pulvinata alleviates cognitive impairment in mice

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          Abstract

          Cognitive impairment (CI) refers to dysfunctional cognition, which encompasses a spectrum of disorders, ranging from mild cognitive impairment to dementia. Any factor that results in cortical damage may cause CI. Total flavonoids of Selaginella pulvinata (TFSP), have shown promising antioxidant and protective effects in animal models. In the present study, mice were intraperitoneally treated with scopolamine, sodium nitrite or 45% ethanol to induce memory impairment, and the effects were assessed using a step-down test. After performing the behavioural test, hippocampal sections were collected for anatomical analysis, and the brain and serum levels of memory-related molecules were evaluated. The results showed that TFSP improved memory in a mouse model of CI significantly. Serum data were consistent with the behavioural results: TFSP increased blood acetylcholine levels through modulation of the acetylcholinesterase and choline acetyltransferase levels. It also ameliorated oxidative stress in neurons, increasing superoxide dismutase, glutathione peroxidase and inhibiting nitric oxide synthase levels in the brain. These results suggest that TFSP may exhibit potential as a clinical treatment for neurodegenerative diseases, including Parkinson's disease, Alzheimer's disease, and senile dementia.

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          The validity of scopolamine as a pharmacological model for cognitive impairment: a review of animal behavioral studies.

          Scopolamine is used as a standard/reference drug for inducing cognitive deficits in healthy humans and animals. Effects are often interpreted in terms of a role of acetylcholine in mnemonic and/or attentional processes. In this paper an overview is given of the effects of scopolamine on animal behavior. Examination of the dose-response curve of systemically administered scopolamine indicates that sensory discrimination and attention are most sensitive to disruption. When higher doses (>0.03mg/kg) are used, deficits in other cognitive and non-cognitive functions (e.g., learning and memory, locomotor activity) are reported. Several behavioral processes (taste aversion, anxiety, short-term memory, attention) are found to be affected after intracerebral injections of scopolamine. It is concluded that effects on learning and memory performance which are observed after higher doses of scopolamine are mediated by (1) primary effects on attention and sensory/stimulus discrimination, (2) non-specific effects on behavior (e.g., locomotor activity, anxiety), and (3) peripheral side-effects (e.g., pupil dilation, salivation). Finally, the validity of scopolamine as a pharmacological model for cognitive impairment is discussed. The use of muscarinic M1 antagonists is suggested as a more selective and effective way of inducing cholinergic-induced cognitive deficits.
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            Improvement of cognitive function and physical activity of aging mice by human neural stem cells over-expressing choline acetyltransferase.

            Aging is characterized by progressive loss of cognitive and memory functions as well as decrease in physical activities. In the present study, a human neural stem cell line (F3 NSC) over-expressing choline acetyltransferase (F3.ChAT), an enzyme responsible for acetylcholine synthesis, was generated and transplanted in the brain of 18-month-old male ICR mice. Four weeks post-transplantation, neurobehavioral functions, expression of ChAT enzyme, production of acetylcholine and neurotrophic factors, and expression of cholinergic nervous system markers in transplanted animals were investigated. F3.ChAT NSCs markedly improved both the cognitive function and physical activity of aging animals, in parallel with the elevation of brain acetylcholine level. Transplanted F3 and F3.ChAT cells were found to differentiate into neurons and astrocytes, and to produce ChAT proteins. Transplantation of the stem cells increased brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF), enhanced expression of Trk B, and restored host microtubule-associated protein 2 and cholinergic nervous system. The results demonstrate that human NSCs over-expressing ChAT improve cognitive function and physical activity of aging mice, not only by producing ACh directly but also by restoring cholinergic neuronal integrity, which might be mediated by neurotrophins BDNF and NGF. Copyright © 2013 Elsevier Inc. All rights reserved.
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              Amentoflavone protects hippocampal neurons: anti-inflammatory, antioxidative, and antiapoptotic effects

              Amentoflavone is a natural biflavone compound with many biological properties, including anti-inflammatory, antioxidative, and neuroprotective effects. We presumed that amentoflavone exerts a neuroprotective effect in epilepsy models. Prior to model establishment, mice were intragastrically administered 25 mg/kg amentoflavone for 3 consecutive days. Amentoflavone effectively prevented pilocarpine-induced epilepsy in a mouse kindling model, suppressed nuclear factor-κB activation and expression, inhibited excessive discharge of hippocampal neurons resulting in a reduction in epileptic seizures, shortened attack time, and diminished loss and apoptosis of hippocampal neurons. Results suggested that amentoflavone protected hippocampal neurons in epilepsy mice via anti-inflammation, antioxidation, and antiapoptosis, and then effectively prevented the occurrence of seizures.
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                Author and article information

                Journal
                Biomed Rep
                Biomed Rep
                BR
                Biomedical Reports
                D.A. Spandidos
                2049-9434
                2049-9442
                August 2020
                09 June 2020
                09 June 2020
                : 13
                : 2
                : 8
                Affiliations
                [1 ]College of Fisheries and Life Science, Hainan Tropical Ocean University, Sanya, Hainan 572022, P.R. China
                [2 ]Department of Biopharmacy, School of Pharmaceutical Sciences, Jilin University, Changchun, Jilin 130022, P.R. China
                [3 ]School of Life and Pharmaceutical Sciences, Dalian University of Technology, Dalian, Liaoning 116024, P.R. China
                [4 ]The Hospital Affiliated to Changchun University of Chinese Medicine, Changchun, Jilin 130021, P.R. China
                [5 ]Department of Biochemistry and Molecular Biology, College of Pharmacy, Henan University of Chinese Medicine, Zhengzhou, Henan 450046, P.R. China
                Author notes
                Correspondence to: Dr Zhengyao Zhang, School of Life and Pharmaceutical Sciences, Dalian University of Technology, 2 Linggong Road, Ganjingzi District, Dalian, Liaoning 116024, P.R. China zhengyaozhang@ 123456dlut.edu.cn
                Article
                BR-0-0-01315
                10.3892/br.2020.1315
                7323453
                32607237
                52487e1f-4fd8-4d67-8b00-9f49426cc320
                Copyright: © Zhang et al.

                This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

                History
                : 12 October 2019
                : 23 April 2020
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                cognitive impairment,total flavonoids of selaginella pulvinata,mouse model

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