scholarly journals Citrus Auraptene Induces Expression of Brain-Derived Neurotrophic Factor in Neuro2a Cells

Molecules ◽  
2020 ◽  
Vol 25 (5) ◽  
pp. 1117 ◽  
Author(s):  
Yoshiko Furukawa ◽  
Yu-suke Washimi ◽  
Ryu-ichi Hara ◽  
Mizuki Yamaoka ◽  
Satoshi Okuyama ◽  
...  
Keyword(s):  
Neurotrophic Factor ◽  
Neuronal Cells ◽  
Brain Derived Neurotrophic Factor ◽  
C6 Glioma Cells ◽  
Published Data ◽  
Dependent Manner ◽  
Bdnf Expression ◽  
Bdnf Mrna ◽  
Neuroprotective Effects ◽  
Neuro2a Cells

(1) Background: Our published data have indicated that (1) auraptene (AUR), a citrus ingredient, has neuroprotective effects on the mouse brain, owing to its ability to suppress inflammation, such as causing a reduction in hyperactivation of microglia and astrocytes; (2) AUR has the ability to trigger phosphorylation (activation) of extracellular signal-related kinase (ERK) and cAMP response element-binding protein (CREB) in neuronal cells; (3) AUR has the ability to induce glial cell line-derived neurotrophic factor (GDNF) synthesis/secretion in rat C6 glioma cells. The well-established fact that the ERK-CREB pathway plays an important role in the production of neurotrophic factors, including GDNF and brain-derived neurotrophic factor (BDNF), prompted us to investigate whether AUR would also have the ability to induce BDNF expression in neuronal cells. (2) Methods: Mouse neuroblastoma neuro2a cells were cultured and the effects of AUR on BDNF mRNA expression and protein content were evaluated by RT-PCR and ELISA, respectively. (3) Results: The levels of BDNF mRNA and secreted BDNF were significantly increased by AUR in a dose- and time-dependent manner in neuro2a cells. (4) Conclusion: The induction of BDNF in neuronal cells might be, in part, one of the mechanisms accounting for the neuroprotective effects of AUR.

scholarly journals OLAHRAGA DAPAT MENINGKATKAN FUNGSI KOGNITIF MELALUI MODULASI EPIGENETIK EKSPRESI GEN BRAIN-DERIVED NEUROTROPHIC FACTOR (BDNF)

2019 ◽  
Author(s):  
Nila Wahyuni ◽  
Made Hendra Satria Nugraha ◽  
Indira Vidiari Juhanna
Keyword(s):  
Cognitive Function ◽  
Epigenetic Regulation ◽  
Learning Process ◽  
Neural Plasticity ◽  
Neurotrophic Factor ◽  
Brain Derived Neurotrophic Factor ◽  
Regulatory Change ◽  
Literature Study ◽  
Bdnf Expression ◽  
Bdnf Mrna

ABSTRACTExercise may improve cognitive function and slow the onset of neurodegeneration, but the underlying mechanism had not yet known certainly. The purpose of this paper is to know the mechanism of exercise in improving cognitive function in terms of biomolecular aspects. The method of this paper is literature study of articles about the benefits of exercise in improving cognitive function in terms of biomolecular aspects. Cognitive function is a function related to perception, learning process, concentration, memory and problem solving. Exercise is useful for improving cognitive function mediated by a neurotropin-brain brain-derived neurotrophic factor (BDNF). BDNF has important role in neural plasticity, nerve excitability, and especially in learning process and memory improving. Exercise can improve cognitive function by inducing increased BDNF expression that occurs through the mechanism of epigenetic regulatory change. The change in epigenetic regulation caused by exercise through DNA methylation, which increase the expression of BDNF mRNA in the hippocampus. The change in epigenetic regulation caused by exercise, which also increase the expression of BDNF mRNA is a histone modification. The increased expression of mRNA in the hippocampus is not only increase synapse plasticity in the hippocampus area but also synapse transmission, which lead to the increasing of molecules expression related to learning and memory.Keywords: Sport, Brain-derived neurotrophic factor (BDNF), Epigenetic.

scholarly journals Dimeric Tacrine (10)-Hupyridone Effectively Combats Alzheimer’s Disease as A Multi-Target-Directed Ligand

2021 ◽  
Author(s):  
Zhenquan Xuan ◽  
Xingmei Gu ◽  
Sicheng Yan ◽  
Yanfei Xie ◽  
Yiying Zhou ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neurotrophic Factor ◽  
Neurodegenerative Disorder ◽  
Brain Derived Neurotrophic Factor ◽  
Huperzine A ◽  
Bdnf Expression ◽  
Neuroprotective Effects ◽  
Aβ Oligomers

Abstract Background Alzheimer’s disease (AD) is a neurodegenerative disorder with multiple pathological features. Therefore, multi-target-directed ligands (MTDLs) strategy has been developed to combat this disease. We have previously designed and synthesized dimeric tacrine (10)-hupyridone (A10E), a novel tacrine derivative with acetylcholinesterase (AChE) inhibition and brain-derived neurotrophic factor (BDNF) activation activity, by linking tacrine and a fragment of huperzine A. However, it was largely unknown whether A10E could act on other AD targets and produce cognition-enhancing ability in AD animal models. Methods Behavioral and biochemical methods were applied to evaluate multi-target cognitive-enhancing effects and mechanisms of A10E in APP/PS1 transgenic mice and β-amyloid (Aβ) oligomers-treated mice. The neuroprotective mechanisms of A10E were explored in SH-SY5Y cells. And the anti-aggregation effects of A10E on Aβ were directly investigated in vitro. Results A10E could prevent cognitive impairments in both APP/PS1 mice and Aβ oligomers-treated mice, with higher potency than tacrine and huperzine A. Moreover, A10E could effectively inhibit Aβ production and deposition, reduce neuroinflammation, enhance brain derived brain-derived neurotrophic factor (BDNF) expression, and elevate cholinergic neurotransmission in vivo. A10E, at nanomolar concentrations, could also inhibit Aβ oligomers-induced neurotoxicity via the activation of the TrkB/Akt pathway. Furthermore, Aβ oligomerization and fibrillization could be directly disrupted by A10E. Conclusion A10E could produce anti-AD neuroprotective effects via multi-target mechanisms, including the inhibition of Aβ aggregation, the activation of the BDNF/TrkB pathway, the reduction of neuroinflammation and the decrease of AChE activity. As MTDLs could produce additional benefits, such as overcoming the deficits of drug combination and enhancing the compliance of AD patients, our results suggested that A10E might be developed as a promising MTDL lead for the treatment of AD.

Is Brain-Derived Neurotrophic Factor: A Common Link Between Neurodegenerative Disorders and Cancer?

2019 ◽  
Vol 16 (4) ◽  
pp. 344-352
Author(s):  
Radhika Khosla ◽  
Avijit Banik ◽  
Sushant Kaushal ◽  
Priya Battu ◽  
Deepti Gupta ◽  
...  
Keyword(s):  
Neurodegenerative Disorders ◽  
Neurotrophic Factor ◽  
Animal Studies ◽  
Neurodegenerative Disorder ◽  
Indirect Evidence ◽  
Brain Derived Neurotrophic Factor ◽  
Common Disease ◽  
Inverse Association ◽  
Bdnf Expression ◽  
Strong Inverse Association

Background: Cancer is a common disease caused by the excessive proliferation of cells, and neurodegenerative diseases are the disorders caused due to the degeneration of neurons. Both can be considered as diseases caused by the dysregulation of cell cycle events. A recent data suggests that there is a strong inverse association between cancer and neurodegenerative disorders. There is indirect evidence to postulate Brain-derived Neurotrophic Factor (BDNF) as a potential molecular link in this association. Discussion: The BDNF levels are found to be downregulated in many neurodegenerative disorders and are found to be upregulated in various kinds of cancers. The lower level of BDNF in Alzheimer’s and Parkinson’s disease has been found to be related to cognitive and other neuropsychological impairments, whereas, its higher levels are associated with the tumour growth and metastasis and poor survival rate in the cancer patients. Conclusion: In this review, we propose that variance in BDNF levels is critical in determining the course of cellular pathophysiology and the development of cancer or neurodegenerative disorder. We further propose that an alternative therapeutic strategy that can modulate BDNF expression, can rescue or prevent above said pathophysiological course. Larger studies that examine this link through animal studies are imperative to understand the putative biochemical and molecular link to wellness and disease.

scholarly journals Modulation of Brain-Derived Neurotrophic Factor (BDNF) Signaling Pathway by Culinary Sage (Salvia officinalis L.)

2021 ◽  
Vol 22 (14) ◽  
pp. 7382
Author(s):  
Nancy Chiang ◽  
Shahla Ray ◽  
Jade Lomax ◽  
Sydney Goertzen ◽  
Slavko Komarnytsky ◽  
...  
Keyword(s):  
Liquid Chromatography ◽  
Neurotrophic Factor ◽  
High Performance ◽  
Memory Function ◽  
Brain Derived Neurotrophic Factor ◽  
Salvia Officinalis ◽  
C6 Glioma Cells ◽  
Medicinal Uses ◽  
Bdnf Signaling ◽  
Salvia Officinalis L

Culinary sage (Salvia officinalis L.) is a common spice plant in the mint family (Lamiaceae) well known for its distinctive culinary and traditional medicinal uses. Sage tea has been used traditionally as a brain-enhancing tonic and extracts from sage have been reported to have both cognitive and memory enhancing effects. Brain-derived neurotrophic factor (BDNF) is an endogenous signaling molecule involved in cognition and memory function. In this study, activity-guided fractionation employing preparative reverse-phase high performance liquid chromatography (RP-HPLC) of culinary sage extracts led to the discovery of benzyl 6-O-β-D-apiofuranosyl-β-D-glucoside (B6AG) as a natural product that upregulates transcription of neurotrophic factors in C6 glioma cells. Purified B6AG showed a moderate dose response, with upregulation of BDNF and with EC50 at 6.46 μM. To better understand the natural variation in culinary sage, B6AG was quantitated in the leaves of several commercial varieties by liquid chromatography-mass spectrometry (LC-MS). The level of B6AG in dried culinary sage was found to range from 334 ± 14 to 698 ± 65 μg/g. This study provided a foundation for future investigations, including quantitative inquiries on the distribution of B6AG within the different plant organs, explorations in optimizing post-harvest practices, and aid in the development of sage varieties with elevated levels of B6AG.

scholarly journals Chronic Exercise Increases Plasma Brain-Derived Neurotrophic Factor Levels, Pancreatic Islet Size, and Insulin Tolerance in a TrkB-Dependent Manner

PLoS ONE ◽  
2014 ◽  
Vol 9 (12) ◽  
pp. e115177 ◽  
Author(s):  
Alberto Jiménez-Maldonado ◽  
Elena Roces de Álvarez-Buylla ◽  
Sergio Montero ◽  
Valery Melnikov ◽  
Elena Castro-Rodríguez ◽  
...  
Keyword(s):  
Pancreatic Islet ◽  
Neurotrophic Factor ◽  
Brain Derived Neurotrophic Factor ◽  
Dependent Manner ◽  
Chronic Exercise ◽  
Insulin Tolerance ◽  
Islet Size

scholarly journals Brain-derived neurotrophic factor enhances spontaneous sleep in rats and rabbits

1999 ◽  
Vol 276 (5) ◽  
pp. R1334-R1338 ◽  
Author(s):  
Tetsuya Kushikata ◽  
Jidong Fang ◽  
James M. Krueger
Keyword(s):  
Growth Factors ◽  
Neurotrophic Factor ◽  
Brain Temperature ◽  
Brain Derived Neurotrophic Factor ◽  
Normal Brain ◽  
Sprague Dawley ◽  
Sleep Regulation ◽  
Bdnf Mrna ◽  
Sprague Dawley Rats ◽  
Intracerebroventricular Injections

Various growth factors are involved in sleep regulation. Brain-derived neurotrophic factor (BDNF) belongs to the neurotrophin family; it and its receptors are found in normal brain. Furthermore, cerebral cortical levels of BDNF mRNA have a diurnal variation and increase after sleep deprivation. Therefore, we investigated whether BDNF would promote sleep. Twenty-four male Sprague-Dawley rats (320–380 g) and 25 male New Zealand White rabbits (4.5–5.5 kg) were surgically implanted with electroencephalographic (EEG) electrodes, a brain thermistor, and a lateral intracerebroventricular cannula. The animals were injected intracerebroventricularly with pyrogen-free saline and, on a separate day, one of the following doses of BDNF: 25 or 250 ng in rabbits; 10, 50, or 250 ng in rats. The EEG, brain temperature, and motor activity were recorded for 23 h after the intracerebroventricular injections. BDNF increased time spent in non-rapid eye movement sleep (NREMS) in rats and rabbits and REMS in rabbits. Current results provide further evidence that various growth factors are involved in sleep regulation.

Antiapoptotic activity maintenance of Brain Derived Neurotrophic Factor and the C fragment of the tetanus toxin genetic fusion protein

2008 ◽  
Vol 3 (2) ◽  
pp. 105-112 ◽  
Author(s):  
Jesús Ciriza ◽  
Marcos García-Ojeda ◽  
Inmaculada Martín-Burriel ◽  
Cendra Agulhon ◽  
Francisco Miana-Mena ◽  
...  
Keyword(s):  
Amyotrophic Lateral Sclerosis ◽  
Neurotrophic Factor ◽  
Tetanus Toxin ◽  
Brain Derived Neurotrophic Factor ◽  
Trophic Factors ◽  
Low Concentrations ◽  
Neuro2a Cells ◽  
Genetic Fusion ◽  
The Brain ◽  
Lateral Sclerosis

AbstractNeurotrophic factors have been widely suggested as a treatment for multiple diseases including motorneuron pathologies, like Amyotrophic Lateral Sclerosis. However, clinical trials in which growth factors have been systematically administered to Amyotrophic Lateral Sclerosis patients have not been effective, owing in part to the short half-life of these factors and their low concentrations at target sites. A possible strategy is the use of the atoxic C fragment of the tetanus toxin as a neurotrophic factor carrier to the motorneurons. The activity of trophic factors should be tested because their genetic fusion to proteins could alter their folding and conformation, thus undermining their neuroprotective properties. For this purpose, in this paper we explored the Brain Derived Neurotrophic Factor (BDNF) activity maintenance after genetic fusion with the C fragment of the tetanus toxin. We demonstrated that BDNF fused with the C fragment of the tetanus toxin induces the neuronal survival Akt kinase pathway in mouse cortical culture neurons and maintains its antiapoptotic neuronal activity in Neuro2A cells.

Dose-related effects of venlafaxine on pCREB and brain-derived neurotrophic factor (BDNF) in the hippocampus of the rat by chronic unpredictable stress

2011 ◽  
Vol 23 (1) ◽  
pp. 20-30 ◽  
Author(s):  
Jing-Jing Li ◽  
Yong-Gui Yuan ◽  
Gang Hou ◽  
Xiang-Rong Zhang
Keyword(s):  
Neurotrophic Factor ◽  
Sucrose Solution ◽  
Brain Derived Neurotrophic Factor ◽  
Rat Hippocampus ◽  
Antidepressant Effect ◽  
High Dose ◽  
Sprague Dawley ◽  
Bdnf Mrna ◽  
Adult Rat ◽  
Element Binding Protein

Background: The molecular pathogenesis of depression and psychopharmacology of antidepressants remain elusive. Recent hypotheses suggest that changes in neurogenesis and plasticity may underlie the aetiology of depression. The hippocampus is affected by depression and shows neuronal remodelling during adulthood.Objective: The present study on the adult rat hippocampus, was to evaluate the dose-related effects of chronic venlafaxine on the expression of brain-derived neurotrophic factor (BDNF) and phosphorylated cyclic-AMP response element binding protein (pCREB).Methods: Sprague-Dawley rats were exposed to a variety of chronic unpredictable stressors (CUSs) to establish a depression model. Rats were treated for either 14 or 28 days with venlafaxine (5 and 10 mg/kg, respectively). The hippocampal expression of pCREB and BDNF mRNA and protein was assessed by using immunohistochemistry, western blotting and reverse transcription polymerase chain reaction (RT-PCR).Results: Rats subjected to CUS procedure consumed less sucrose solution compared with non-stressed rats. The CUS influenced exploratory activity resulting in a reduction of the motility counts. Chronic low dose (5 mg/kg, 14 and 28 days), but not high dose (10 mg/kg, 14 and 28 days) of venlafaxine treatment increased the expression of pCREB and BDNF mRNA and protein in the CUS rat hippocampus.Conclusion: Neuronal plasticity-associated proteins such as pCREB and BDNF play an important role both in stress-related depression and in antidepressant effect.

scholarly journals Interferon beta-1a induces expression of brain-derived neurotrophic factor in human T lymphocytes in vitro and not in vivo

2020 ◽  
Vol 15 (1) ◽  
pp. FNL38 ◽  
Author(s):  
Zarlascht Karmand ◽  
Hans-Peter Hartung ◽  
Oliver Neuhaus
Keyword(s):  
T Cell ◽  
Neurotrophic Factor ◽  
Serum Levels ◽  
Brain Derived Neurotrophic Factor ◽  
Peripheral Blood Lymphocytes ◽  
T Cell Proliferation ◽  
Bdnf Expression ◽  
Healthy Donors

Aim: To detect IFN β-1a-induced expression of brain-derived neurotrophic factor (BDNF) to undermine the hypothesis of IFN β-1a-associated neuroprotection in multiple sclerosis (MS). Methods: The influence of IFN β-1a on in vitro activated peripheral blood lymphocytes from healthy donors was tested. Proliferation analyses were made to detect T-cell growth. BDNF expression was measured by standard ELISA. To assess the influence of IFN β-1a on BDNF expression in vivo, BDNF serum levels of MS patients treated with IFN β-1a were compared with those of untreated patients. Results: IFN β-1a inhibited T-cell proliferation dose dependently. It induced BDNF expression at middle concentrations. MS patients treated with IFN β-1a exhibited significantly lower BDNF serum levels than untreated patients. Conclusion: IFN β-1a may promote neuroprotection by inducing BDNF expression, but its importance in vivo remains open.

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