• Biomedical Science Letters
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• v.17 no.3
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• pp.267-271
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• 2011

P19 cells are pluripotent embryonal carcinoma cells and can be differentiated into neuronal cell type by treatment with retinoic acid (RA) and aggregation culture. Cannabinoids are the active components of Cannabis sativa and they have diverse pharmacologic activities, such as pain control, anti-inflammatory effects, neuro-protection effects and tumor regression. Cannabinoids also involved in neuronal proliferation, migration, differentiation and survival in developing brain. Here, we studied the role of cannabinoids on neuronal differentiation of P19 cells. Treatment with cannabinoids increased the neuronal differentiation induced by RA and also promoted transcriptional activity of neurogenin 1, key transcription factor for neuronal differentiation of P19 cells. These results suggest that the cannabinoids can accelerate neuronal differentiation of P19 cells.

• The Korea Journal of Herbology
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• v.21 no.4
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• pp.77-84
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• 2006

Objectives : To evaluate the neuroprotective effects of modified Bo-Yang-Hwan-O-Tang (BHT), we investigated the neuronal death protection effects to oxidative damages in N2a neuroblastoma cells. Methods : To study the cytotoxic effect of BHT on N2a neuronal cells, the cell viability was determined by MTT assay. To investigate the neuronal death protection of BHT, N2a neuronal cells were induced oxidative damages by H2O2, and assayed the cell viability and DNA fragmentation. We also investigated DPPH free radical scavenging effects of BHT by tube test. Results : In MTT assay, $500{\mu}g/ml$ of BHT was not showed cytotoxic effect on N2a neuronal cells. BHT protected N2a neuronal cells from H2O2-induced cell death in a dose-dependent manner. BHT also protected N2a neuronal cells from H2O2-induced DNA fragmentation. BHT scavenged DPPH free radicals in a dose-dependent manner. Conclusion : These data suggest that BHT may have strong anti-oxidant effects through the free radical scavenging and neuroprotective effects in neuronal cells.

• The Korea Journal of Herbology
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• v.21 no.4
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• pp.85-92
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• 2006

Objectives : To evaluate the neuroprotective effects of added Bo-Yang-Hwan-Oh-Tang (BHT), we investigated the neuronal death protection effects to oxidative damages in SH-SY5Y neuronal cells. Methods : To study the cytotoxic effects of BHT on SH-SY5Y cells, the cell viability was determined by MTT assay. To investigate the neuronal death protection of BHT, SH-SY5Y cells were induced oxidative damages by $H_2O_2$ and then assayed the cell viability and DNA fragmentation. We also investigated DPPH free radical scavenging effect of BHT by tube test. Results : In MTT assay, $1000{\mu}g/ml$ of BHT was not showed the cytotoxic effect on SH-SY5Y cells. BHT protected SHSY5Y cells from $H_2O_2-induced $ neuronal cell death in a dose-dependent manner. BHT also protected SH-SY5Y cells from $H_2O_2-induced$ DNA fragmentation. BHT effectively scavenged DPPH free radicals in a dose-dependent manner. Conclusion : These data suggest that BHT may have strong antioxidant effects through the free radical scavenging and neuroprotective effects in human neuronal cells.

• The Journal of Internal Korean Medicine
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• v.40 no.3
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• pp.425-442
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• 2019

Objectives: This study aimed to reveal the pharmacological properties of the newly prescribed herbal mixture, Chenmadansamgamibokhap-tang(CDBT), against hypoxia-induced neuronal cell injury (especially mouse hippocampal neuronal cell line, HT-22 cells) and their corresponding mechanisms. Methods: A cell-based in vitro experiment, in which a hypoxia condition induced neuronal cell death, was performed. Various concentrations of the CDBT were pre-treated to the HT-22 cells for 4 h before 18 h in the hypoxia chamber. The glial cell BV-2 cells were stimulated with $IFN{\gamma}$ and LSP to produce inflammatory cytokines and reactive oxygen species. When the neuronal HT-22 cells were treated with this culture solution, the drug efficacy against neuronal cell death was examined. Results: CDBT showed cytotoxicity in the normal condition of HT-22 cells at a dose of $125{\mu}g/mL$ and showed a protective effect against hypoxia-induced neuronal cell death at a dose of $31.3{\mu}g/mL$. CDBT prevented hypoxia-induced neuronal cell death in a dose-dependent manner in the HT-22 cells by regulating $HIF1{\alpha}$ and cell death signaling. CDBT prevented neuronal cell death signals and DNA fragmentation due to the hypoxia condition. CDBT significantly reduced cellular oxidation, cell death signals, and caspase-3 activities due to microglial cell activations. Moreover, CDBT significantly ameliorated LPS-induced BV-2 cell activation and evoked cellular oxidation through the recovery of redox homeostasis. Conclusions: CDBT cam be considered as a vital therapeutic agent against neuronal cell deaths. Further studies are required to reveal the other functions of CDBT in vivo or in the clinical field.

• The Journal of Korean Medicine
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• v.23 no.1
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• pp.120-132
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• 2002

Objectives : The purpose of this investigation was to evaluate the effect of Goomicheongsim-won Extracts on E20 corticells and P7 cerebellar cells exposed to hypoxia, and the effect on neuronal protection by elimination of Rhinoceros unicornis L. and/or Orpiment $As_2S_3$. Methods : P7 cerebellar cells were grown in various concentrations of KM-A, KM-B, KM- C and KM-D. On 7 DIV (day in vitro), cells were exposed to hypoxia (98% $N_2/5%{;}CO_2,{\;}3{\;}hr,{\;}37^{\circ}C$) and normoxia, and then further incubated for 3 days. Neuronal viabilities were expressed as percentages of control. E20 cortical cells were grown in various concentrations of KM-A, KM-B, KM-C, and KM-D. On 7 DIV, cells were exposed to hypoxia and normoxia, and then further incubated for 3 and 7 days. Results : I. The effect of KM-A on neuronal protection was significantly increased P7 cerebellar granule cells and E20 cortical cells on normoxia and hypoxia. 2. The effect of KM-B on neuronal protection was increased P7 cerebellar granule cells on normoxia, but was significantly decreased P7 cerebellar granule cells on hypoxia. The effect of KM-B on neuronal protection was non-significantly increased E20 cortical cells on normoxia and hypoxia. 3. The effect of KM-C on neuronal protection was non-significantly increased P7 cerebellar granule cells on normoxia and hypoxia and was decreased (p=0.058) on hyperconcentration of the extracts in normoxia. The effect of KM-C on neuronal protection was significantly increased P7 cerebellar granule cells and E20 cortical cells on normoxia and hypoxia (10 DIV), and the effect was E20 cortical cells on normoxia (14 DIV), non-significantly increased E20 cortical cells on hypoxia (14DIV). 4. The effect of KM-D on neuronal protection was increased P7 cerebellar granule cells on normoxia but was not on hyperconcentration of the extracts, was significantly decreased on hyperconcentration of the extracts in hypoxia. The effect of KM-D on neuronal protection was significantly increased E20 cortical cells on normoxia and was significantly increased E20 cortical cells increased on hypoxia (10 DIV). Conclusions : Goomicheongsim-won extracts had applicable effect on E20 corticells and P7 cerebellar cells exposed to hypoxia. The effect on neuronal protection by elimination of Rhinoceros unicornis L. and/or Orpiment $As_2S_3$ was changed.

• 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.

• 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.

• Rapid Communication in Photoscience
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• v.3 no.3
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• pp.48-49
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• 2014

For in vitro myelination system, Schwann cells and neuronal cells of rat were cocultured. Schwann cells and neuronal cells, respectively, were obtained from dorsal root ganglion of rat embryos (E15). This method includes four steps: first step of suspension of the embryonic dorsal root ganglion cells, second step of addition of anti-mitotic cocktail, third step of purification of dorsal root cells, and fourth step of addition of Schwann cells to dorsal root ganglion cells. We made a highly purified population of myelination in a short period through this procedure and identified myelination basic protein using antibody of myelination basic protein.

• Biomolecules & Therapeutics
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• v.29 no.6
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• pp.605-614
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• 2021

Autophagy is an important degradative pathway that eliminates misfolded proteins and damaged organelles from cells. Autophagy is crucial for neuronal homeostasis and function. A lack of or deficiency in autophagy leads to the accumulation of protein aggregates, which are associated with several neurodegenerative diseases. Compared with non-neuronal cells, neurons exhibit rapid autophagic flux because damaged organelles or protein aggregates cannot be diluted in post-mitotic cells; because of this, these cells exhibit characteristic features of autophagy, such as compartment-specific autophagy, which depends on polarized structures and rapid autophagy flux. In addition, neurons exhibit compartment-specific autophagy, which depends on polarized structures. Neuronal autophagy may have additional physiological roles other than amino acid recycling. In this review, we focus on the characteristics and regulatory factors of neuronal autophagy. We also describe intracellular selective autophagy in neurons and its association with neurodegenerative diseases.