• Biomolecules & Therapeutics
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• v.24 no.3
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• pp.338-345
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• 2016

Neurodegenerative diseases are often associated with oxidative damage in neuronal cells. This study was conducted to investigate the neuro-protective effect of methanolic (MeOH) extract of Perilla frutescens var. japonica and its one of the major compounds, rosmarinic acid, under oxidative stress induced by hydrogen peroxide ($H_2O_2$) in C6 glial cells. Exposure of C6 glial cells to $H_2O_2$ enhanced oxidative damage as measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and thiobarbituric acid-reactive substance assays. The MeOH extract and rosmarinic acid prevented oxidative stress by increasing cell viability and inhibiting cellular lipid peroxidation. In addition, the MeOH extract and rosmarinic acid reduced $H_2O_2-indcued$ expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) at the transcriptional level. Moreover, iNOS and COX-2 protein expression was down-regulated in $H_2O_2-indcued$ C6 glial cells treated with the MeOH extract and rosmarinic acid. These findings suggest that P. frutescens var. japonica and rosmarinic acid could prevent the progression of neurodegenerative diseases through attenuation of neuronal oxidative stress.

• The Journal of Internal Korean Medicine
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• v.28 no.3
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• pp.586-596
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• 2007

Objectives : This study aimed to investigate the underlying protective mechanism of Rhizoma Arisaematis(RA) on 3-NP-induced Cytotoxicity in rat C6 glial cells. Methods : We investigated treatment ofC6 cells with 20mM 3-NP and pretreatment with RA to cause loss of cell viability. and morphological change. which was associated with elevation of ROS level. increase in Bax/Bcl2 ratio and HIF-a protein expression Results : RA inhibited 3-NP-induced cell death in C6 glial cells and inhibited the changes of the : MMPT (mitochondria membrane potential transition) and inhibited the decrease of mitochondria complex II activity and 3-NP-induced ROS generation in C6 cells. And RA decreased the activity of HIF-a and Bax. and increased the activity of $Bcl_2$ in C6 glial cells Conclusions : RA markedly protects C6 glial cells from 3-NP-induced oxidative injury.

• Korean Journal of Pharmacognosy
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• v.46 no.2
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• pp.109-115
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• 2015

This study was investigated the radical scavenging effect and the protective activity of caffeic acid (CA) against oxidative stress. CA showed strong 1,1-diphenyl-2-picrylhydrazyl radical (DPPH) and hydroxyl radical ( OH) scavenging activity, showing 42.00% and 87.22% at 5 μM concentration of DPPH and ·OH scavenging activity, respectively. Furthermore, we studied protective activity of CA from amyloid beta (A${\beta}$_25-35) and lipopolysaccharide (LPS) induced neuronal cell damage and neuronal inflammation using C6 glial cells. The treatment of A${\beta}$_25-35 to C6 glial cell showed declines in cell viability and high generation levels of reactive oxygen species (ROS). However, the treatment of CA increased cell viability. The treatment of 5 ${{\mu}M}$ CA led to the elevation of cell viability from 59.28% to 81.22%. In addition, the production of ROS decreased cellular levels of ROS by the treatment of CA. The treatment of LPS to C6 glial cells increased significant elevation of nitric oxide (NO) production, while CA decreased NO production significantly. The production of NO increased by the treatment of LPS to 131.08%, while CA at the concentration of 1 ${{\mu}M}$ declined the NO production to 104.86%. The present study indicated thatCA attenuated A${\beta}$_25-35-induced neuronal oxidative stress and inflammation by LPS, suggesting as a promising agent for the neurodegenerative diseases.

• Korean Journal of Biological Psychiatry
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• v.22 no.2
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• pp.34-39
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• 2015

Mood disorder is a common psychiatric illness with a high lifetime prevalence in the general population. A serious problem such as suicide is commonly occurring in the patients with depression. Till now, the monoamine hypothesis has been the most popular theory of pathogenesis for depression. However, the more specific pathophysiology of depression and cellular molecular mechanism underlying action of commercial antidepressants have not been clearly defined. Several recent studies demonstrated that glial cells, especially astrocytes, are a promising answer to the pathophysiology of depression. In this article, current understanding of biology and molecular mechanisms of glial cells in the pathology of mood disorder and new research on the pathophysiology of depression will be discussed.

• The Korean Journal of Physiology and Pharmacology
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• v.6 no.5
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• pp.235-239
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• 2002

It has been reported that lovastatin induced cell death and suppressed proliferation in various cell lines. In this study, we examined whether the cytotoxic effects of lovastatin could be prevented by Bcl-2 or $Bcl-_{XL}$ in C6 glial cells. Overexpression of human Bcl-2 or $Bcl-_{XL}$ prevented lovastatin $(25{\mu}M)-induced$ changes such as DNA fragmentation, chromatin condensation, disruption of cell membrane, and cleavage of poly (ADP-ribose) polymerase. Lovastatin-induced inhibition of cell proliferation was unaffected by Bcl-2 or $Bcl-_{XL}$ overexpression. These results suggest that Bcl-2 and $Bcl-_{XL}$ can prevent lovastatin-induced apoptosis in C6 glial cells, though the inhibition of proliferation remains unaffected by these proteins.

• The Journal of Internal Korean Medicine
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• v.34 no.2
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• pp.178-191
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• 2013

Objectives : In this study, we made an effort to investigate the protective mechanism of Ukgan-san (UGS) extracts on hypoxia-induced C6 glial cell death. Methods : The cell viability was assessed by 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide (MMT) assay and cell morphological changes were analysed with microscope after staining with crystal violet (CV). Reactive oxygen species (ROS) formation was assessed by flow cytometer after staining with 2'7'-dichlorofluorescein diacetate (DCF-DA). We also analyzed expression of hypoxia-inducible factor-1 alpha (HIF-$1{\alpha}$) and p53, processing of procaspase-3 and procyclic acidic repetitive protein (PARP) by western blot method. Results : We estimated the elevated cell viability by UGS extract on $CoCl_2$-induced C6 glial cells. UGS attenuated $CoCl_2$-induced ROS formation in C6 glial cells and also showed a protective activity compared to antioxidants and exhibited abrogation of LDH-released by $CoCl_2$. UGS suppressed the typical apoptotic cell death markers, caspase-3 and PARP activation. UGS inhibited $CoCl_2$-induced HIF-1${\alpha}$ expression which is known as a major regulator for hypoxia-induced cell death, and suppressed p53 expression. Conclusions : These results suggest that UGS extract contains protective constituents for hypoxia-induced C6 glial cell death.

• Journal of Life Science
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• v.23 no.10
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• pp.1183-1191
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• 2013

Human apurinic/apyrimidinic endonuclease (APEX-1) is a multifunctional protein that is capable of repairing abasic sites and single-strand breaks in damaged DNA. In addition, it serves as a redox-modifying factor for a number of transcription factors. Identifying the transcriptional targets of APEX-1 is essential for understanding how it affects various cellular outcomes. Expression array analysis was used to identify glial cell-derived neurotropic factor receptor ${\alpha}1$ ($GFR{\alpha}1$), which is an encoding receptor for the glial cell-derived neurotropic factor (GDNF) family, the expression of which is induced by APEX-1. A target of GDNF/$GFR{\alpha}$ signaling, c-Src (Tyr418) was strongly phosphorylated by GNDF in the APEX-1 expressing cells. Moreover, GDNF initiated cell proliferation, measured by counting the number of cells, in the APEX-1 expressing cells. Importantly, the down-regulation of APEX-1 by siRNA caused a marked reduction in the $GFR{\alpha}1$ expression level, and it reduced the ability of GDNF to phosphorylate c-Src (Tyr418) and stimulate cell proliferation. These results demonstrate an association between APEX-1 and GDNF/$GFR{\alpha}$ signaling and suggest a potential molecular mechanism for the involvement of APEX-1 in cell survival and proliferation.

• Proceedings of the Korean Society of Toxicology Conference
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• 2002.05a
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• pp.14-23
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• 2002

The nervous system consists of two types of cells, which are neurons and glial cells. Among the glial cells, oligodendrodendrocytes and schwann cells form myelin sheaths in the central nervous system (CNS) and the peripheral nervous system (PNS), respectively. The major function of myelin in vertebrates is to insulate axonal and help action potential travel faster.(omitted)

• Korean Journal of Agricultural Science
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• v.45 no.3
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• pp.509-519
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• 2018

This study was investigated the anti-oxidant property and neuro-protective effect of Cirsium japonicum var. maackii (CJM) against oxidative stress in hydrogen peroxide ($H_2O_2$)-induced C6 glial cells. We measured the 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical, hydroxyl radical (${\cdot}OH$), and superoxide ($O_2{^-}$) radical scavenging activities of an ethanol extract and four fractions [n-Butanol, ethyl acetate (EtOAc), $CHCl_3$, and n-Hexane] from CJM. The results of this study show that the extract and all fractions from CJM had a dose-dependent DPPH radical scavenging activity. In particular, the EtOAc fraction exhibited the strongest scavenging effect with 88.23% at a concentration of $500{\mu}g/mL$. In addition, the EtOAc fraction from CJM also effectively scavenged ${\cdot}OH$ radicals and $O_2{^-}$ radicals, compared to other extract and fractions. In C6 glial cells, $H_2O_2$ markedly decreased the cell viability as well as increased lactate dehydrogenase (LDH) release and reactive oxygen species (ROS) production. However, the EtOAc fraction of CJM attenuated the cellular damage from the oxidative stress by elevating the cell viability and inhibiting the LDH release and ROS over-production compared with the $H_2O_2$-treated control group. Our findings indicate that the EtOAc fraction from CJM has antioxidant effect and neuro-protective effect against oxidative stress, suggesting that it can be used as a natural antioxidant and therapeutic agent for the prevention of neurodegenerative disorders.

• The Journal of Internal Korean Medicine
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• v.23 no.2
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• pp.191-201
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• 2002

Objectives : This study was designed to investigate the effects of Yukmijihwang-tang on contusion of the mice induced with medicine. Methods : I observed the effects of light and electron microscopes. and examined hematological changes and VEGF-immunohistochemistry. Results : Hematology: Leukocytes were increased significantly in a control group of mice compared with the experimental group. Light microscope : A few neurons were condensed in the 7-day experimental group, but condensed remarkedly in the 3-day control group. Most glial cells were observed in the 3-day experimental group. Edema and dilatation of vessels occurred significantly in the 3-day control group, and these results occurred weakly in the 7-day experimental group. VEGF-immunohistochemistry : VEGF-immunohistochemical reactivity for the glial cells was the highest in the 3-day experimental group, and immunoreactivity for the vessels and neurons highly increased in the 7-day experimental group. Electron microscope : In the 3-day control group, protoplasmic astrocytes concerned with angiogenesis contained weakly developed rough endoplasmic reticulum. and a few of glial filaments were observed. In the 7-day experimental group, the bundles of glial filaments were found in the cytoplasmic process of astrocytes. Conclusion : medication using Yukmijihwang-tang of mice contused by medical stress is highly effective in inflamatory response, curing cell damage and angiogenesis.