• The Korean Journal of Physiology and Pharmacology
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• v.11 no.2
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• pp.37-43
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• 2007

Adenosine has been reported to provide cytoprotection in the central nervous systems as well as myocardium by activating cell surface adenosine receptors. However, the exact target and mechanism of its action still remain controversial. The present study was performed to examine whether adenosine has a protective effect against $A{\beta}$-induced injury in neuroglial cells. The astrocyte-derived human neuroglioma cell line, A172 cells, and $A{\beta}_{25{\sim}35}$ were employed to produce an experimental $A{\beta}$-induced glial cell injury model. Adenosine significantly prevented $A{\beta}$-induced apoptotic cell death. Studies using various nucleotide receptor agonists and antagonists suggested that the protection was mediated by $A_1$ receptors. Adenosine attenuated $A{\beta}$-induced impairment in mitochondrial functional integrity as estimated by cellular ATP level and MTT reduction ability. In addition, adenosine prevented $A{\beta}$-induced mitochondrial permeability transition, release of cytochrome c into cytosol and subsequent activation of caspase-9. The protective effect of adenosine disappeared when cells were pretreated with 5-hydroxydecanoate, a selective blocker of the mitochondrial ATP-sensitive $K^+$ channel. In conclusion, therefore we suggest that adenosine exerts protective effect against $A{\beta}$-induced cell death of A172 cells, and that the underlying mechanism of the protection may be attributed to preservation of mitochonarial functional integrity through opening of the mitochondrial ATP-sensitive $K^+$ channels.

• 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.

• BMB Reports
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• v.47 no.12
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• pp.679-684
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• 2014

GM-CSF plays a role in the nervous system, particularly in cases of injury. A therapeutic effect of GM-CSF has been reported in rat models of various central nervous system injuries. We previously showed that GM-CSF could enhance long-term recovery in a rat spinal cord injury model, inhibiting glial scar formation and increasing the integrity of axonal structure. Here, we investigated molecular the mechanism(s) by which GM-CSF suppressed glial scar formation in an in vitro system using primary astrocytes treated with TGF-${\beta}$. GM-CSF repressed the expression of chondroitin sulfate proteoglycan (CSPG) core proteins in astrocytes treated with TGF-${\beta}$. GM-CSF also inhibited the TGF-${\beta}$-induced Rho-ROCK pathway, which is important in CSPG expression. Finally, the inhibitory effect of GM-CSF was blocked by a JAK inhibitor. These results may provide the basis for GM-CSF's effects in glial scar inhibition and ultimately for its therapeutic effect on neural cell injuries.

• Proceedings of the PSK Conference
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• 2002.04a
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• pp.174.2-175
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• 2002

• Journal of Applied Biological Chemistry
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• v.60 no.2
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• pp.141-147
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• 2017

Radical scavenging effect and protective activity against oxidative stress of Acer okamotoanum were investigated. A. okamotoanum was extracted with methanol (MeOH) and then fractionated with n-BuOH, ethyl acetate (EtOAc), methylene chloride and n-hexane fractions. The MeOH extract and fractions showed strong 1,1-diphenyl-2-picrylhydrazyl and superoxide radical scavenging activity. Among the MeOH extract and fractions, the EtOAc fraction showed the strongest radical scavenging activity. In addition, total phenolic and flavonoid contents of EtOAc fraction was higher than other extract and fractions. Furthermore, we investigated the neuroprotective effect of the MeOH extract and fractions from A. okamotoanum against oxidative stress under cellular system using C6 glial cell. The C6 glial cells showed a decrease in cell viability and high production of reactive oxygen species (ROS) by the treatment of amyloid $beta_{25-35}$ ($A{\beta}_{25-35}$). However, with the treatment of the MeOH extract and fractions, it significantly increased the cell viability and inhibited the overproduction of ROS by $A{\beta}_{25-35}$. In particular, the EtOAc fraction led to significantly increase the cell viability and decrease the generation of ROS against oxidative stress by $A{\beta}_{25-35}$. The current study indicated that A. okamotoanum demonstrated antioxidative and neuroprotective effects. In particular, the EtOAc fraction which attributed a strong protective activity against oxidative stress.

• Journal of Nutrition and Health
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• v.10 no.2
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• pp.5-11
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• 1977

The mature human braun contains over 10 billion nerve cells (neurons), whose functions are directly related to the acquisition, transfer, processing, analysis, and utilization of all the information. There are also billions of glial cells, which serve primarily to support and to maintain the integrity of the neuron network and to synthesize an essential fatty strucfure, myelin. In the human brain DNA content therefore cell number rises rapidly until birth and then more slowly until $5{\sim}6$ months of age, when it reaches a maximum. While glial cells may be replaced, the more important nerve cell neurons can never be replaced once they are formed. Humans are born with their full complement of neurons and every neuron is as old as each individual. Thus prenatal malnutrition can seriously affect a person's entire life by severely inhibiting the production of neurons before birth.It has been demonstrated that in humans severe malnutrition during the fetal period and in infancy is associated with intellectual impairment. Severely malnourished children have brains smaller than average size and have been found to have $15{\sim}20%$ fewer brain cells than wellnourished childen. There is growing body of literature pointing to malnutrition as a cause of abnormal behavior as evidence that suggests these abnormalities may produce chromosomal damage that may persist forever. Although cognitive development in children is affected by multiple environmental factors, nutrition certainly deaerves more attention than it has received.

• Restorative Dentistry and Endodontics
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• v.22 no.2
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• pp.782-791
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• 1997

Glial fibrillary acidic protein(GFAP) are a group of intermediate filaments that are distributed in the cytoplasm of many type of glial cells. The purpose of this study was to determine change of GFAP immunoreactivity(GFAP-IR) in rat trigeminal ganglion satellite cells in response to pulp exposure. The immunohistochemistry was carried out using the avidinbiotin-peroxidase complex(ABC) method and subsequently stained with AEC(3-aminoethyl-9-carbasol). 1. Contol group; Central root astrocytes had strong GFAP-IR, but ganglion satellite cells occasionlly had GFAP-IR. This reaction patterns of ganglion satellite cells was not concenturated in any specific region of trigeminal ganglion. 2. Three day pulp exposure group; There was a highly GFAP-IR in satellite cells of trigeminal ganglion in maxillary region. GFAP-IR in neighboring mandibular and ophthalmic regions was less intense compared to maxillary region. 3. Seven day pulp exposure group; In this group, GFAP-IR that was increased compared to control group was seen in the maxillary region. But GFAP-IR was less intense compared to three day pulp exposure group. These results suggest that GFAP in satellite cell increase in specific region of trigeminal ganglion after pulp exposure and offer useful tool in trigeminal pain research.

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.117.2-117.2
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• 2003

The mechanism by which lead enters glial cells was examined. The uptake of lead reached saturation when assays were performed in buffers at pH 5.5 and 7.4. The Vmax and Km was 2.7 pmoles/mg protein/min and 13.4 M in the buffer at pH 7.4, respectively, whereas the Vmax and Km was 329 fmoles/mg and 8.2 M in the buffer at pH 5.5, respectively. Uptake in a buffer at pH 5.5 but not at pH 7.4 was inhibited by iron. Cells treated with the iron chelator desferoxamine displayed higher levels of the divalent metal transporter mRNA and protein. (omitted)

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.326.2-327
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• 2002

Glial cell-derived neurotrophic factor (GDNF) is a potent neurotrophic factor that enhances survival of midbrain doparminergic neuron. GDNF and its receptors are widely distributed in brain and are believed to be involved in the control of neuron survival and differentiation. In this study, we examined the effect of GDNF on proliferation and migration of Hs683 human glioma cells. GDNF markedly enhances proliferation and migration of Hs683 cells in a dose-dependent manner. (omitted)

• Proceedings of the Korean Society of Toxicology Conference
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• 2002.11b
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• pp.140-140
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• 2002

Glial cell-derived neurotrophic factor (GDNF) is a potent neurotrophic factor that enhances survival of midbrain doparminergic neuron and is a member of the transforming growth factor-b superfamily. GDNF and its receptors are widely distributed in brain and are believed to be involved in the control of neuron survival, proliferation and differentiation.(omitted)