7, 8, 3’-Trihydroxyflavone Promotes Neurite Outgrowth and Protects Against Bupivacaine-Induced Neurotoxicity in Mouse Dorsal Root Ganglion Neurons

Shi, Hao-Hong; Luo, Xingjing

doi:10.12659/msm.896961

Cited by 10 publications

(4 citation statements)

References 19 publications

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“…Since we expected THF to at least match the effect of BDNF, the lack of any effect from the THF treatment is surprising. More so since recently, in in vitro studies in mice and rats, THF has been found to be effective in promoting neurite outgrowth in dorsal root ganglion explants [57] and cochlear SGC explants [47] in a reportedly TrkB-dependent manner. Frick et al [47] compared the effects of BDNF with THF on neurite outgrowth.…”

Section: The Elusive Effect Of Thfmentioning

confidence: 99%

BDNF Outperforms TrkB Agonist 7,8,3′-THF in Preserving the Auditory Nerve in Deafened Guinea Pigs

et al. 2020

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In deaf subjects using a cochlear implant (CI) for hearing restoration, the auditory nerve is subject to degeneration, which may negatively impact CI effectiveness. This nerve degeneration can be reduced by neurotrophic treatment. Here, we compare the preservative effects of the naturally occurring tyrosine receptor kinase B (TrkB) agonist brain-derived neurotrophic factor (BDNF) and the small-molecule TrkB agonist 7,8,3′-trihydroxyflavone (THF) on the auditory nerve in deafened guinea pigs. THF may be more effective than BDNF throughout the cochlea because of better pharmacokinetic properties. The neurotrophic compounds were delivered by placement of a gelatin sponge on the perforated round window membrane. To complement the histology of spiral ganglion cells (SGCs), electrically evoked compound action potential (eCAP) recordings were performed four weeks after treatment initiation. We analyzed the eCAP inter-phase gap (IPG) effect and measures derived from pulse-train evoked eCAPs, both indicative of SGC healthiness. BDNF but not THF yielded a significantly higher survival of SGCs in the basal cochlear turn than untreated controls. Regarding IPG effect and pulse-train responses, the BDNF-treated animals exhibited more normal responses than both untreated and THF-treated animals. We have thus confirmed the protective effect of BDNF, but we have not confirmed previously reported protective effects of THF with our clinically applicable delivery method.

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Section: The Elusive Effect Of Thfmentioning

confidence: 99%

BDNF Outperforms TrkB Agonist 7,8,3′-THF in Preserving the Auditory Nerve in Deafened Guinea Pigs

et al. 2020

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“…General anaesthetics are divided into inhaled and intravenous types; they mainly inhibit cerebral cortical activity, which are represented by propofol and N 2 O 5 . However, animal studies have found that almost all clinically used intravenous anaesthetics can result in neurodegenerative and abnormal synapses during critical periods of brain development, leading to late behavioural changes and cognitive dysfunction 6,7 . Furthermore, the anaesthetics, including propofol, have been proven to induce the apoptosis of nerve cells whilst exerting its benefits, especially in paediatric surgery, which can cause irreversible damage to developmental neurons 8 .…”

Section: Introductionmentioning

confidence: 99%

“…5 However, animal studies have found that almost all clinically used intravenous anaesthetics can result in neurodegenerative and abnormal synapses during critical periods of brain development, leading to late behavioural changes and cognitive dysfunction. 6,7 Furthermore, the anaesthetics, including propofol, have been proven to induce the apoptosis of nerve cells whilst exerting its benefits, especially in paediatric surgery, which can cause irreversible damage to developmental neurons. 8 Therefore, studying the side effects of anaesthetics and exploring the underlying mechanisms will be helpful for improving the safety of anaesthesia.…”

Section: Introductionmentioning

confidence: 99%

Propofol induces oxidative stress and apoptosis in vitro via regulating miR‐363‐3p/CREB signalling axis

Yao

Zhang

2020

Cell Biochemistry & Function

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Propofol, a generally used anaesthetic in patients care, has been proven to induce neurotoxicity. Studies have shown that miR-363-3p was closely related to neurological dysfunction, and the up-regulated miR-363-3p was recognized to be participate in propofol-induced neurotoxicity. However, the mechanisms and functions of miR-363-3p in propofol-induced neurotoxicity remain rarely reported. The aim of our research was to clarify the potential effects of miR-363-3p in neurotoxicity induced by propofol. SH-SY5Y cells were treated with propofol, miR-363-3p inhibitor or sh-CREB. quantitative real-time polymerase chain reaction and western blotting were applied to detect the expression of miR-363-3p, CREB, Bax, Bcl-2, cleaved caspase-9 and cleaved caspase-3 at the mRNA and/or protein level, respectively. The levels of lactate dehydrogenase (LDH), superoxide dismutase (SOD) and malondialdehyde (MDA) in cell supernatant were detected using different kits. Flow cytometry and MTT assay were applied for assessing the functions of miR-363-3p and CREB on cell ability in cellular activity and apoptotic rate. In addition, Bioinformatic analysis and luciferase assay verified the relationship between 3 0-UTR of CREB and miR-363-3p. Our data indicated that the cell viability decreased with the increasing propofol concentration. Bioinformatic analysis and luciferase assay suggested that 3 0-UTR of transcript of CREB might be a binding site of miR-363-3p, and miR-363-3p could negatively regulate the expression of CREB. The changes in reactive oxygen species, LDH, SOD and MDA suggested that propofol mediates oxidative stress and apoptosis via modulating miR-363-3p/CREB axis. Propofol induces oxidative stress and apoptosis via affecting miR-363-3p/CREB axis in SH-SY5Y cells, suggesting miR-363-3p down-regulation may act as a novel strategy to ameliorate the propofol-induced neurotoxicity. Significance of the study: The present study demonstrated that propofol induces oxidative stress and apoptosis via affecting miR-363-3p/CREB axis in SH-SY5Y cells, suggesting miR-363-3p down-regulation may act as a novel strategy to ameliorate the propofol-induced neurotoxicity.

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“…Spinal DRGn are afferent neurons of peripheral nervous system and primary neurons of sensory conduction system. With the increasing research on the nervous system, such as the pain mechanism of diseases [1][2][3], spinal cord injury repair [4,5], electrophysiological research [6][7][8][9], it is necessary to establish a simple and easy-to-obtain primary nerve cell culture scheme.…”

Section: Introductionmentioning

confidence: 99%

A New Method for Primary Culture of Mouse Dorsal Root Ganglion Neurons

Dong

et al. 2018

Preprint

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In order to establish a simple and highly purified method for primary culture of mouse dorsal root ganglion neurons(DRGn), in this study, the DRGn of young mice were obtained by collagenase type I and trypsin digestion.Then the DRGn were obtained by immunocytochemical staining of mouse neuron specific enolase (NSE) monoclonal antibody, while using flow cytometry to further detect the positive rates of DRGn. The cultured primary DRGn grew well and had a purity of about 83.72%. The DRGn survival time was 60 days when cultured in DMEM medium containing nerve growth factor (NGF). The culture scheme is simple and stable, and a large number of high purity DRGn could be cultured, which provides a reliable model for further study of nerve cells.

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7, 8, 3’-Trihydroxyflavone Promotes Neurite Outgrowth and Protects Against Bupivacaine-Induced Neurotoxicity in Mouse Dorsal Root Ganglion Neurons

Cited by 10 publications

References 19 publications

BDNF Outperforms TrkB Agonist 7,8,3′-THF in Preserving the Auditory Nerve in Deafened Guinea Pigs

BDNF Outperforms TrkB Agonist 7,8,3′-THF in Preserving the Auditory Nerve in Deafened Guinea Pigs

Propofol induces oxidative stress and apoptosis in vitro via regulating miR‐363‐3p/CREB signalling axis

A New Method for Primary Culture of Mouse Dorsal Root Ganglion Neurons

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