Neuroprotective effect of Asparagus racemosus root extract via the enhancement of brain-derived neurotrophic factor and estrogen receptor in ovariectomized rats

Brain-derived neurotrophic factor (BDNF) has potent effects on neuronal survival and plasticity during development and after injury. In the nervous system, neurons are considered the major cellular source of BDNF. We demonstrate here that in addition, activated human T cells, B cells, and monocytes secrete bioactive BDNF in vitro. Notably, in T helper (Th)1- and Th2-type CD4+ T cell lines specific for myelin autoantigens such as myelin basic protein or myelin oligodendrocyte glycoprotein, BDNF production is increased upon antigen stimulation. The BDNF secreted by immune cells is bioactive, as it supports neuronal survival in vitro. Using anti-BDNF monoclonal antibody and polyclonal antiserum, BDNF immunoreactivity is demonstrable in inflammatory infiltrates in the brain of patients with acute disseminated encephalitis and multiple sclerosis. The results raise the possibility that in the nervous system, inflammatory infiltrates have a neuroprotective effect, which may limit the success of nonselective immunotherapies.

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Neuroprotective effects of dehydroepiandrosterone (DHEA) in rat model of Alzheimer's disease.

Acta Biochimica Polonica ◽

10.18388/abp.2011_2218 ◽

2011 ◽

Vol 58 (4) ◽

Cited By ~ 28

Author(s):

Hanan F Aly ◽

Fateheya M Metwally ◽

Hanaa H Ahmed

Keyword(s):

Oxidative Stress ◽

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Body Weight ◽

Rat Model ◽

Neurotrophic Factor ◽

Intraperitoneal Administration ◽

Brain Derived Neurotrophic Factor ◽

Ovariectomized Rats ◽

Antioxidant Enzyme Activities

The current study was undertaken to elucidate a possible neuroprotective role of dehydroepiandrosterone (DHEA) against the development of Alzheimer's disease in experimental rat model. Alzheimer's disease was produced in young female ovariectomized rats by intraperitoneal administration of AlCl(3) (4.2 mg/kg body weight) daily for 12 weeks. Half of these animals also received orally DHEA (250 mg/kg body weight, three times weekly) for 18 weeks. Control groups of animals received either DHAE alone, or no DHEA, or were not ovariectomized. After such treatment the animals were analyzed for oxidative stress biomarkers such as hydrogen peroxide, nitric oxide and malondialdehyde, total antioxidant capacity, reduced glutathione, glutathione peroxidase, glutathione reductase, superoxide dismutase and catalase activities, antiapoptotic marker Bcl-2 and brain derived neurotrophic factor. Also brain cholinergic markers (acetylcholinesterase and acetylcholine) were determined. The results revealed significant increase in oxidative stress parameters associated with significant decrease in the antioxidant enzyme activities in Al-intoxicated ovariectomized rats. Significant depletion in brain Bcl-2 and brain-derived neurotrophic factor levels were also detected. Moreover, significant elevations in brain acetylcholinesterase activity accompanied with significant reduction in acetylcholine level were recorded. Significant amelioration in all investigated parameters was detected as a result of treatment of Al-intoxicated ovariectomized rats with DHEA. These results were confirmed by histological examination of brain sections. These results clearly indicate a neuroprotective effect of DHEA against Alzheimer's disease.

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Modulatory effect of simvastatin on redox status, caspase-3 expression, p-protein kinase B (p-Akt) and brain derived neurotrophic factor (BDNF) in ethanol-induced neurodegeneration

Canadian Journal of Physiology and Pharmacology ◽

10.1139/cjpp-2020-0360 ◽

2020 ◽

Author(s):

nahla anas nasef ◽

Walaa Arafa Keshk ◽

salwa elmelegy ◽

ahmed abdallah ◽

wafaa ibrahim

Keyword(s):

Protein Kinase ◽

Neurotrophic Factor ◽

Caspase 3 ◽

Protein Kinase B ◽

Neuroprotective Effect ◽

Brain Derived Neurotrophic Factor ◽

Ethanol Solution ◽

Biochemical Changes ◽

Lipid Lowering ◽

P Protein

Neurodegenerative diseases are a common cause of morbidity and mortality worldwide with oxidative stress, inflammation and protein aggregation represent the main underlying mechanisms that ultimately lead to cell death. Ethanol has shown strong neurodegenerative consequences in experimental animal brains. Statins are a class of lipid-lowering drugs with many pleotropic effects. Therefore, the aim of the present study was to explore the modulatory effect of simvastatin (10 mg/kg/day) before and after the development of neurodegeneration (for 55 and 25 days, respectively) on redox state, caspase-3 expression, p-protein kinase B (p-Akt) and brain derived neurotrophic factor (BDNF) in ethanol (15% ethanol solution for 55 day) induced neurodegeneration. Seventy female Albino Swiss mice were included and randomly divided into 5 groups: control (c) group; ethanol (E) group; (ES) group treated with simvastatin from the first day of ethanol intake; (E+S) group treated with simvastatin after neurodegeneration development; and simvastatin (S) group. Administration of simvastatin from the first day improved the biochemical changes, suppressed apoptosis, induced autophagy and neurogenesis. However, its administration after the development of neurodegeneration resulted in partial improvement. The histopathological findings confirmed the biochemical changes. In conclusion; simvastatin has a neuroprotective effect against the development of ethanol-induced neurodegeneration and its progression.

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Effects of exercise on mature or precursor brain-derived neurotrophic factor pathways in ovariectomized rats

Molecular Medicine Reports ◽

10.3892/mmr.2017.6614 ◽

2017 ◽

Vol 16 (1) ◽

pp. 435-440 ◽

Cited By ~ 6

Author(s):

Joon-Ki Park ◽

Young-Pyo Hong ◽

Sam-Jun Lee

Keyword(s):

Neurotrophic Factor ◽

Brain Derived Neurotrophic Factor ◽

Ovariectomized Rats

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The Neuroprotective Mechanism of Low-Frequency rTMS on Nigral Dopaminergic Neurons of Parkinson’s Disease Model Mice

Parkinson s Disease ◽

10.1155/2015/564095 ◽

2015 ◽

Vol 2015 ◽

pp. 1-8 ◽

Cited By ~ 2

Author(s):

Qiaoyun Dong ◽

Yanyong Wang ◽

Ping Gu ◽

Rusheng Shao ◽

Li Zhao ◽

...

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Cell Line ◽

Glial Cell ◽

Neurotrophic Factor ◽

Dopaminergic Neuron ◽

Neuroprotective Effect ◽

Low Frequency ◽

Brain Derived Neurotrophic Factor ◽

Low Frequency Rtms

Background. Parkinson’s disease is a neurodegenerative disease in elder people, pathophysiologic basis of which is the severe deficiency of dopamine in the striatum. The purpose of the present study was to evaluate the neuroprotective effect of low-frequency rTMS on Parkinson’s disease in model mice.Methods. The effects of low-frequency rTMS on the motor function, cortex excitability, neurochemistry, and neurohistopathology of MPTP-induced Parkinson’s disease mice were investigated through behavioral detection, electrophysiologic technique, high performance liquid chromatography-electrochemical detection, immunohistochemical staining, and western blot.Results. Low-frequency rTMS could improve the motor coordination impairment of Parkinson’s disease mice: the resting motor threshold significantly decreased in the Parkinson’s disease mice; the degeneration of nigral dopaminergic neuron and the expression of tyrosine hydroxylase were significantly improved by low-frequency rTMS; moreover, the expressions of brain derived neurotrophic factor and glial cell line derived neurotrophic factor were also improved by low-frequency rTMS.Conclusions. Low-frequency rTMS had a neuroprotective effect on the nigral dopaminergic neuron which might be due to the improved expressions of brain derived neurotrophic factor and glial cell line-derived neurotrophic factor. The present study provided a theoretical basis for the application of low-frequency rTMS in the clinical treatment and recovery of Parkinson’s disease.

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