Identifying inducers of BDNF gene expression from pharmacologically validated compounds; antipyretic drug dipyrone increases BDNF mRNA in neurons

Fukuchi, Mamoru

doi:10.1016/j.bbrc.2020.02.019

Cited by 11 publications

(9 citation statements)

References 24 publications

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“…An open eld test was conducted to analyze the locomotor activity and explore the novel environment (Wills 1965). Many studies depict the decline in the number of line crossing activity (OFT) in CUMS group, re ecting a depressive-like behaviors (Fukuchi 2020).…”

Section: Discussionmentioning

confidence: 99%

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Neuroprotective Potential of Sodium Orthovanadate in a Mouse Model of Chronic Unpredictable Mild Stress.

Joshi

Akhtar

Kuhad

et al. 2021

Preprint

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Depression is a psychiatric disorder characterized by low-esteem, anhedonia, social deficit, and lack of interest. Decreased BDNF and impaired TrKB signaling have been found to be associated in depression. Moreover, oxidative stress in the brain and subsequent reduction of BDNF have a prominent role in psychiatric disorders. In our study, depressive-like behavior was induced in mice by chronic unpredictable mild stress (CUMS) model. Further, sodium orthovanadate (SOV), a protein tyrosine phospahatase was used as a test drug as it is reported to stimulate BDNF levels. Sodium orthovanadate (SOV-5 mg/kg, 10 mg/kg) and fluoxetine (10 mg/kg) were given to mice orally for 21 days prior 30 minutes of stress induction. Various behavioral studies like tail suspension test (TST), open field test (OFT), and sucrose preference test (SPT); biochemical analyses for corticosterone, reduced glutathione (GSH), lipid peroxidation (LPO), superoxide dismutase (SOD), nitric oxide (NO) and ELISA for BDNF were performed. Body weight was measured on a weekly basis. The behavioral tests reflected depressive-like behavior in CUMS, which was attenuated by SOV and fluoxetine. SOV (10 mg/kg) significantly decreased malondialdehyde levels, NO, whereas increased GSH and SOD in both the cortex and hippocampus. Besides, ELISA revealed the elevation of BDNF levels in the treatment groups compared with the disease group (CUMS). Therefore, the treatment with SOV appeared to reverse both oxidative and nitrosative stress. Elevated BDNF level was associated with attenuation of depressive-like behaviors and serum corticosterone levels. The findings of this preliminary study indicates that SOV has potential to restore mood and social interaction in depression and so further molecular mechanisms will be warranted for clinical translation.

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Section: Discussionmentioning

confidence: 99%

“…Major Depressive Disorder (MDD) is one of the most prevalent, recurrent, and debilitating psychopathology forms. Epidemiological surveys indicate that the lifetime prevalence of MDD is 16.6%, with estimates as high as 21.3% in women (LeMoult and Gotlib 2019).…”

Section: Introductionmentioning

confidence: 99%

Neuroprotective Potential of Sodium Orthovanadate in a Mouse Model of Chronic Unpredictable Mild Stress.

Joshi

Akhtar

Kuhad

et al. 2021

Preprint

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“…Although the structural and functional changes implicated in the relationship between depression and neurodegeneration seem to be highly complex, excitingly, several studies have shown altered BDNF production and secretion in a variety of neurodegenerative diseases as well as in depression [ 136 ]. Overall, BDNF is one of the key molecules modulating and linking brain plasticity, and the neuroplasticity hypothesis postulates that the loss of BDNF plays a major role in the pathophysiology of poststroke depression and depression with AD [ 137 , 138 ]. Similarly, in a short review, while providing evidence of shared biological substrates between PD and depression, neuroplasticity was underscored by the roles of BDNF [ 139 ].…”

Section: Discussionmentioning

confidence: 99%

Applications of Acupuncture Therapy in Modulating the Plasticity of Neurodegenerative Disease and Depression: Do MicroRNA and Neurotrophin BDNF Shed Light on the Underlying Mechanism?

Xia

Zhao

et al. 2020

Neural Plasticity

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As the global population ages, the incidence of neurodegenerative diseases has risen. Furthermore, it has been suggested that depression, especially in elderly people, may also be an indication of latent neurodegeneration. Stroke, Alzheimer’s disease (AD), and Parkinson’s disease (PD) are usually accompanied by depression. The urgent challenge is further enforced by psychiatric comorbid conditions, particularly the feeling of despair in these patients. Fortunately, as our understanding of the neurobiological substrates of maladies affecting the central nervous system (CNS) has increased, more therapeutic options and novel potential biological mechanisms have been presented: (1) Neurodegenerative diseases share some similarities in their pathological characteristics, including changes in neuron structure or function and neuronal plasticity. (2) MicroRNAs (miRNAs) are small noncoding RNAs that contribute to the pathogenesis of diverse neurological disease. (3) One ubiquitous neurotrophin, brain-derived neurotrophic factor (BDNF), is crucial for the development of the nervous system. Accumulating data have indicated that miRNAs not only are related to BDNF regulation but also can directly bind with the 3′-UTR of BDNF to regulate BDNF and participate in neuroplasticity. In this short review, we present evidence of shared biological substrates among stroke, AD, PD, and depression and summarize the possible influencing mechanisms of acupuncture on the neuroplasticity of these diseases. We discuss neuroplasticity underscored by the roles of miRNAs and BDNF, which might further reveal the potential biological mechanism of neurodegenerative diseases and depression by acupuncture.

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“…Primary cultures of rat cortical neurons were prepared from cerebral cortices of Sprague-Dawley rats at embryonic day 17 [Japan SLC (Shizuoka, Japan)], as described previously [ 12 , 13 ]. All animal care and experimental protocols were approved by the Animal Experiment Committee of Takasaki University of Health and Welfare (Authorization No.…”

Section: Methodsmentioning

confidence: 99%

“…One microgram of total RNA, which was isolated and purified using an ISOSPIN Cell & Tissue RNA kit [Nippongene (Tokyo, Japan)], was reverse-transcribed into cDNA using a PrimeScript 1st strand cDNA Synthesis Kit [Takara Bio Inc. (Shiga, Japan)], according to the manufactures’ instructions. Real-time PCR was carried out using SYBR Select Master Mix (Thermo Fisher Scientific), as described previously [ 12 , 13 ]. PCR thermal profiles included initial heating at 50 °C for 2 min then at 95 °C for 2 min, followed by 45 cycles of denaturation at 95 °C for 45 s, annealing at 57 °C for 45 s, and extension at 72 °C for 1 min.…”

Section: Methodsmentioning

confidence: 99%

Aminothioneine, a product derived from golden oyster mushrooms (Pleurotus cornucopiae var. citrinopileatus), activates Ca2+ signal-mediated brain-derived neurotrophic factor expression in cultured cortical neurons

Watanabe

Mitazaki

Fukuda

et al. 2021

Biochemistry and Biophysics Reports

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Ameliorating reduced brain-derived neurotrophic factor (BDNF) expression or maintaining high BDNF levels in the brain has been suggested to improve brain function in neurological diseases and prevent aging-related brain dysfunction. In this study, we found that a food-derived product, Aminothioneine® (AT), which is prepared from the extract of golden oyster mushrooms ( Pleurotus cornucopiae var. citrinopileatus ), increased Bdnf mRNA expression levels in primary rat cortical neuron cultures. Ergothioneine (ET) comprises more than 1% in AT and is an active constituent of AT, and ET has been reported to increase neurotrophin-4/5, but not BDNF, expression levels in neural stem cells. ET also did not affect Bdnf mRNA expression in cultured cortical neurons, suggesting that AT contains other active constituents that induce Bdnf mRNA expression in neurons. AT-induced Bdnf mRNA expression was completely blocked by d -(−)-2-Amino-5-phosphonopentanoic acid but partially blocked by nicardipine, U0126, and FK506. This result suggested that N -methyl- d -aspartate receptor-derived Ca 2+ signals, including those mediated by extracellular signal-regulated kinase/mitogen-activated protein kinase and calcineurin, are the main contributors to Bdnf mRNA induction. In addition, AT increased cAMP-response element-binding protein (CREB) phosphorylation and the nuclear localization of CREB-regulated transcriptional coactivator 1 in neurons. Thus, AT can increase Bdnf mRNA expression via Ca 2+ signal-induced CREB-dependent transcription in neurons. Because AT is a food-derived product, increasing and/or maintaining BDNF levels in the brain by daily intake of the product could be possible, which may be beneficial for neurological and aging-related disorders.

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Identifying inducers of BDNF gene expression from pharmacologically validated compounds; antipyretic drug dipyrone increases BDNF mRNA in neurons

Cited by 11 publications

References 24 publications

Neuroprotective Potential of Sodium Orthovanadate in a Mouse Model of Chronic Unpredictable Mild Stress.

Neuroprotective Potential of Sodium Orthovanadate in a Mouse Model of Chronic Unpredictable Mild Stress.

Applications of Acupuncture Therapy in Modulating the Plasticity of Neurodegenerative Disease and Depression: Do MicroRNA and Neurotrophin BDNF Shed Light on the Underlying Mechanism?

Aminothioneine, a product derived from golden oyster mushrooms (Pleurotus cornucopiae var. citrinopileatus), activates Ca2+ signal-mediated brain-derived neurotrophic factor expression in cultured cortical neurons

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