• Journal of the Korean Society of Food Culture
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• v.36 no.6
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• pp.633-639
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• 2021

Raphanus sativus var. hortensis f. raphanistroides Makino (Korean wild radish [WR]) are root vegetables belonging to the Brassicaceae family. These radish species mostly grow in sea areas in Asia, where they have been traditionally used as a medicinal food to treat various diseases. To investigate the effect of WR on neuronal cell death in SH-SY5Y cells, beta-amyloid was used to develop the cell death model. WR attenuated neuronal cell death in SH-SY5Y and regulated the mitogen-activated protein kinase (MAPK) signaling. WR extract also inhibited acetylcholinesterase inhibitor activity. Additionally, the WR treatment group ameliorated the behavior of the memory-impaired mice in a scopolamine-induced mouse model. In the behavior test, WR treated mice showed shorter escape latency and swimming distance and improved the platform-crossing number and the swimming time within the target quadrant. Furthermore, WR prevented histological loss of neurons in hippocampal CA1 regions induced by scopolamine. This study shows that WR can prevent memory impairment which may be a crucial way for the prevention and treatment of memory dysfunction and neuronal cell death.

• Korean Journal of Microbiology
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• v.42 no.1
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• pp.73-76
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• 2006

Neuronal precursor cells may provide for cell replacement or gene delivery vehicles in neurodegenerative disease therapy. One impediment to treating neuronal diseases is finding ways to introduce genes into neurons effectively. It is shown here that fiber-modified adenovirus vector delivered gene to neuronal precursor as well as differentiated neuronal cells more efficiently than first-generation adenoviral vector. Moreover, fiber-modified adenoviral vector transduced precursor cells retained the potential for differentiation into neurons and glia in vitro. These results show the potential of modified adenoviral vector in the improved gene delivery to neurons in direct gene therapy protocols. In addition it holds promise for the use of genetically manipulated stem cells for the therapy of neuronal diseases.

• Biomolecules & Therapeutics
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• v.18 no.1
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• pp.24-31
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• 2010

Taurine, 2-aminoethanesulfonic acid, is an abundant free amino acid present in brain cells and exerts many important biological functions such as anti-convulsant, modulation of neuronal excitability, regulation of learning and memory, anti-aggressiveness and anti-alcoholic effects. In the present study, we investigated to explore whether taurine has any protective actions against oxidative stress-induced damages in neuronal cells. ERK I/II regulates signaling pathways involved in nitric oxide (NO) and reactive oxygen species (ROS) production and plays a role in the regulation of cell growth, and apoptosis. We have found that taurine significantly inhibited AMPA induced cortical depolarization in the Grease Gap assays using rat cortical slices. Taurine also inhibited AMPA-induced neuronal cell damage in MTT assays in the differentiated SH-SY5Y cells. When the neuronal cells were treated with $H_2O_2$, levels of NO were increased; however, taurine pretreatment decreased the NO production induced by $H_2O_2$ to approximately normal levels. Interestingly, taurine treatment stimulated ERK I/II activity in the presence of AMPA or $H_2O_2$, suggesting the potential role of ERK I/II in the neuroprotection of taurine. Taken together, taurine has significant neuroprotective actions against AMPA or $H_2O_2$ induced damages in neuronal cells, possibly via activation of ERK I/II.

• Journal of Ginseng Research
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• v.30 no.2
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• pp.57-63
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• 2006

One of the various signaling agents in the animal cells is the simple ion called calcium, $Ca^{2+}$.$Ca^{2+}$ controls almost everything that animals do, including fertilization, secretion, metabolism, muscle contractions, heartbeat, learning, memory stores, and more. To do all of this, $Ca^{2+}$ acts as an intracellular messenger, relaying information within cells to regulate their activity. In contrast, the maintenance of intracellular high $Ca^{2+}$ concentrations caused by various excitatory agents or toxins can lead to the disintegration of cells (necrosis) through the activity of $Ca^{2+}$-sensitive protein-digesting enzymes. High concentrations of calcium have also been implicated in the more orderly programs of cell death known as apoptosis. Because this simple ion, acts as an agent for cell birth, life and death, to coordinate all of these functions, $Ca^{2+}$ signalings should be regulated precisely and tightly. Recent reports have shown that ginsenosides regulate directly and indirectly intracellular $Ca^{2+}$ level with differential manners between neuronal and non-neuronal cells. This brief review will attempt to survey how ginsenosides differentially regulate intracellular $Ca^{2+}$ signaling mediated by various ion channels and receptor activations in neuronal and non-neuronal cells.

• Proceedings of the Korean Biophysical Society Conference
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• 2002.06b
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• pp.46-46
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• 2002

Cdk5, a neuronal Cdc2-like kinase, exhibits a variety of functions in neuronal differentiation and neurocytoskeleton dynamics as well as neuronal degeneration and cell death. However, its role in retinoic acid (RA)-induced differentiation has not been reported yet. We newly found that RA treatment of SK-N-BE(2)C, human neuroblastoma, increased expression of Cdk5 concomitantly with a neuronal specific activator, p35.(omitted)

• Laboraroty Animal Research
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• v.33 no.3
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• pp.244-250
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• 2017

${\alpha}$-Synuclein is abundantly expressed in neuronal tissue, plays an essential role in the pathogenesis of neurodegenerative disorders, and exerts a neuroprotective effect against oxidative stress. Cerebral ischemia causes severe neurological disorders and neuronal dysfunction. In this study, we examined ${\alpha}$-synuclein expression in middle cerebral artery occlusion (MCAO)-induced cerebral ischemic injury and neuronal cells damaged by glutamate treatment. MCAO surgical operation was performed on male Sprague-Dawley rats, and brain samples were isolated 24 hours after MCAO. We confirmed neurological behavior deficit, infarction area, and histopathological changes following MCAO injury. A proteomic approach and Western blot analysis demonstrated a decrease in ${\alpha}$-synuclein in the cerebral cortices after MCAO injury. Moreover, glutamate treatment induced neuronal cell death and decreased ${\alpha}$-synuclein expression in a hippocampal-derived cell line in a dose-dependent manner. It is known that ${\alpha}$-synuclein regulates neuronal survival, and low levels of ${\alpha}$-synuclein expression result in cytotoxicity. Thus, these results suggest that cerebral ischemic injury leads to a reduction in ${\alpha}$-synuclein and consequently causes serious brain damage.

• Journal of Korean Neurosurgical Society
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• v.30 no.9
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• pp.1059-1064
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• 2001

Objective : 6R-Tetrahydrobiopterin(BH4) is a cofactor for the aromatic amino acid hydroxylases which is essential for the biosynthesis of catecholamines and serotonin. It also acts as a cofactor for nitric oxide synthase, and stimulates the release of some neurotransmitters such as dopamine, serotonin, acetylcholine and glutamate. Recently, it has been reported that BH4 could induce cellular proliferation and enhance neuronal survival. This study was performed to investigate the antioxidative effect of BH4 on the various oxidative insults in mouse cerebral cortical cell cultures. Methods : Iron ion(FeCl2), zinc ion(ZnCl2), sodium nitroprusside(SNP) and buthionine sulfoximine(BSO, a glutathione depletor) were used as oxidants. Cell death was assessed by measurement of lactate dehydrogenase efflux to bathing media at the end of exposure. Result : All 4 oxidants induced neuronal cell death associated with cell body swelling, which was markedly inhibited by trolox($100{\mu}M$), a vitamin E analog. BH4($10-100{\mu}M$) markedly inhibited the neuronal cell death induced by all 4 oxidants($20{\mu}M\;Cu^{2+}$, $20{\mu}M\;Zn^{2+}$, $1{\mu}M$ SNP or 1mM BSO). However, BH4 failed to inhibit the neuronal cell death induced by 24hr exposure to $20{\mu}M$ NMDA. Conculsion : These results suggest that BH4 has antioxidative action independently of any actions of enzyme cofactor.

• Journal of Microbiology and Biotechnology
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• v.28 no.1
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• pp.40-49
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• 2018

We evaluated the antioxidant activity and neuronal cell-protective effect of fucoidan extract from Ecklonia cava (FEC) on hydrogen peroxide ($H_2O_2$)-induced cytotoxicity in PC-12 and MC-IXC cells to assess its protective effect against oxidative stress. Antioxidant activities were examined using the ABTS radical scavenging activity and malondialdehyde-inhibitory effect, and the results showed that FEC had significant antioxidant activity. Intracellular ROS contents and neuronal cell viability were investigated using the DCF-DA assay and MTT reduction assay. FEC also showed remarkable neuronal cell-protective effect compared with vitamin C as a positive control for both $H_2O_2$-treated PC-12 and MC-IXC cells. Based on the neuronal cell-protective effects, mitochondrial function was analyzed in PC-12 cells, and FEC significantly restored mitochondrial damage by increasing the mitochondrial membrane potential (${\Delta}{\Psi}m$) and ATP levels and regulating mitochondrial-mediated proteins (p-AMPK and BAX). Finally, the inhibitory effects against acetylcholinesterase (AChE), which is a critical hydrolyzing enzyme of the neurotransmitter acetylcholine in the cholinergic system, were investigated ($IC_{50}$ value = 1.3 mg/ml) and showed a mixed (competitive and noncompetitive) pattern of inhibition. Our findings suggest that FEC may be used as a potential material for alleviating oxidative stress-induced neuronal damage by regulating mitochondrial function and AChE inhibition.

• Toxicological Research
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• v.23 no.1
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• pp.33-38
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• 2007

Zinc is an endogenous transition metal that can be synaptically released during neuronal activity. However, zinc may contribute to the neuropathology associated with a variety of conditions. Carnosine expressed in glial cells can modulate the effects of zinc on neuronal excitability as a zinc chelator. We hypothesize that carnosine may protect against neurotoxicity of zinc in cortical neuronal cells. The cortical neuronal cells from newborn rats were prepared and exposed to zinc chloride and/or carnosine at various concentrations. Zinc at the doses of 0 to $500{\mu}M$ decreased neuronal cell viability in a dose-dependent manner. Additionally, at the concentrations of 100 and $200{\mu}M$, it significantly decreased cell viability in an exposed time-dependent manner (p < 0.05). Treatment with carnosine at the concentrations of 20 and $200{\mu}M$ significantly increased neuronal cell proliferation by approximately 14% and 20%, respectively, compared to the control (p < 0.05). At the concentrations of 100 and $200{\mu}M$ zinc, $20{\mu}M$ carnosine significantly increased the viability of neuronal cells by 18.3% and 12.1 %, and $200{\mu}M$ carnosine also increased it by 33.5% and 28.6%, respectively, compared to the normal control group (p < 0.01). These results suggest that carnosine at a physiologically relevant level may protect against zinc-mediated toxicity in neuronal cells as an endogenous neuroprotective agent.

• Korean Journal of Clinical Laboratory Science
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• v.47 no.1
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• pp.51-58
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• 2015

Ethanol has long been implicated in triggering apoptotic neurodegeneration. Alcohol also may indirectly harm the fetus by imparing the mother's physiology. We examined the effects of ethanol on immature brain of mice. Three-weeks-old female ICR strain mice daily intraperitoneally injected with ethanol at the concentration of 4 and 20% in saline for 0, 6, and 24 hours and 1 and 4 weeks. The mice were weighted and sacrificed, and the brains were ectomized for the present histological, immunohistochemical and TUNEL assays. Based on the histologic hematoxylin and eosin stain, immunohistochemical expression of glutamate receptor protein and neuronal cell adhesion molecule (NCAM) were evaluated. The cerebral cortex of the ethanol-treated group showed few typical symptoms of apoptosis such as chromosome condensation and disintegration of the cell bodies. TUNEL staining revealed DNA fragmentation in the 6 and 24 hours. This results demonstrated that acute ethanol administration causes neuronal cell death. I found that either glutamate receptor inhibition or activation could induce cerebellar degeneration as ethanol effect. Neuronal death also can be induced by excess activity of certain neurotransmitter, including glutamate. Neurons must establish cell-to-cell contact during growth and development in order to survive, migrate to their final destination, and develop appropriate connections with neighboring cell. Purkinje cell in cerebellar are especially vulnerable to the cell death and degeneration. After ethanol treatment in cerebellar, NCAM had decreased by 4 weeks. This result suggest that apoptosis seems to be involved in the slow elimination of neuron and cerebellar degeneration.