• Title/Summary/Keyword: glial cell

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Glucose Oxidase/glucose Induces Apoptosis in C6 Glial Cells via Mitochondria-dependent Pathway

  • PARK Min Kyu;KIM Woo Sang;LEE Young Soo;KANG Young Jin;CHONG Won Seog;KIM Hye Jung;SEO Han Geuk;LEE Jae Heun;CHANG Ki Churl
    • Biomolecules & Therapeutics
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    • v.13 no.4
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    • pp.207-213
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    • 2005
  • It has been proposed that reactive oxygen species (ROS), mainly superoxide anion ($O_2^-$) and hydrogen peroxide ($H_2O_2$), may mediate oxidative stress. Production of $H_2O_2$ during oxidative phosphorylation, inflammation, and ischemia can cause oxidative stress leading to cell death. Although glucose oxidase (GOX) in the presence of glucose continuously generates $H_2O_2$, it is not clear whether GOX produces apoptotic cell death in C6 glial cells. Thus, we investigated the mechanism by which GOX induces cell death. Cells were incubated with different concentration of GOX in the presence of glucose where cell viability, TUNEL and DNA ladder were analyzed. Results indicated that GOX exhibited cytotoxicity in a dose dependent manner by MTT assay. TUNEL positive cell and DNA laddering showed that GOX-induced cytotoxicity was due to apoptosis. Western blot analysis also showed that the cleaved caspase-3 level was detected in the GOX-treated cells at 10 mU/ml and increased dramatically at 30 mU/ml. Cleaved PARP also appeared at 10 mU/ml and lasted at 20 or 30 mU/ml of GOX. Cytochrome c level was increased by GOX dose dependently, which was contrast to Bcl-2 expression level. These results suggest that GOX induces apoptosis through caspase-3 activation, which followed by cytochrome c release from mitochondria through regulating of Bcl-2 level.

Effects of Fetal Mesencephalic Cell Grafts on the Intrastriatal 6-hydroxydoapmine Lesioned Rats

  • Joo, Wan Seok;Nam, Eun-Joo;Im, Heh-ln;Jung, Jin-Ah;Lee, Eun-Sun;Hwang, Yu-Jin;Kim, Yong-Sik
    • The Korean Journal of Physiology and Pharmacology
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    • v.8 no.5
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    • pp.245-251
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    • 2004
  • The effects of fetal mesencephalic cell grafts on the restoration of nigrostriatal dopaminergic function were studied in the intrastriatal 6-hydroxydopamine-lesioned rats. Four weeks after lesioning, transplantation of ventral mesencephalic cells from embryonic day 14 fetuses showed the number of tyrosine hydroxylase (TH) positive cells and fiber outgrowth in the grafted striatum, and significantly ameliorated symptomatic motor behavior of the animals, as determined by apomorphine-induced rotation. Furthermore, in substantia nigra pars compacta (SNc), the numbers of TH + cells and fibers were markedly restored. Dopamine content of ipsilateral SNc was close to that of contralateral SNc $(91.9{\pm}9.8%)$ in the transplanted animals, while the ratio was approximately 32% in sham-grafted animals. These results indicate that grafted cells restored the activity for the dopaminergic neurons located in SNc, although they were transplanted into striatum. In addition, we showed that the implanted fetal cells expressed high level of glial cell line-derived neurotrophic factor (GDNF), suggesting that the transplanted fetal cells might serve as a dopamine producer and a reservoir of neurotrophic factors. These results may be helpful in consideration of the therapeutic transplantation at early stage of PD.

Effects of Sokmyeung-tang(SMT) on the Protection of C6 Glial Cells and Ischemic Brain Damage (속명탕(續命湯)이 C6 glial cell 보호 및 허혈성 뇌손상에 미치는 영향)

  • An, Ga-Yong;Choi, Eun-Hee;Kim, In-Soo;Kang, Seong-Sun;Lee, Young-Soo;Hong, Seok;Jeon, Sang-Yun
    • The Journal of Internal Korean Medicine
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    • v.32 no.1
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    • pp.43-55
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    • 2011
  • Objectives : Sokmyeung-tang(SMT) has been used for treatment of CVA in traditional oriental medicine, so this study was designed to evaluate the effect of SMT's protection on brain cell damage against the oxidative stress that was affected by CVA, We also investigated the effect of motor function improvement and neurotrophic factor in ischemic cerebral damaged rats. Methods : We measured cell viability after administrating SMT, chemicals(Paraquat, SNP, rotenone, and $H_2O_2$) which cause oxidative stress, and both SMT and chemicals. We carried out neurobehavioral evaluation(Rotarod test, Beam-walking test, postural reflex test) and observed BDNF (brain-derived neurotrophic factor) expression by injecting SMT into ischemic cerebral damaged rat. Results : Through this study, we observed the following three results. First, brain cell death caused by paraquat, rotenone, and $H_2O_2$ significantly decreased with the treatment of SMT. Second, neuronal movement function in ischemic cerebral damaged rats was significantly improved by the treatment of SMT. Third, BDNF in ischemic cerebral damaged rats increased with the treatment of SMT. Conclusions : SMT protects brain cells from damage induced by oxidative stress (Paraquat, rotenone, $H_2O_2$). SMT also improves neuronal movement function and increases BDNF in ischemic cerebral damaged rats.

The Protective Effects of Protocatechuic Acid from Momordica charantia against Oxidative Stress in Neuronal Cells (여주 활성 물질 Protocatechuic Acid의 신경세포의 산화적 스트레스에 대한 개선 효과)

  • Choi, Jung Ran;Choi, Ji Myung;Lee, Sanghyun;Cho, Kye Man;Cho, Eun Ju;Kim, Hyun Young
    • Korean Journal of Pharmacognosy
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    • v.45 no.1
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    • pp.11-16
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    • 2014
  • Protocatechuic acid is an active phenolic acid compound from Momordica charantia. In this study, we investigated the protective effect of protocatechuic acid against oxidative stress under cellular system using C6 glial cell. The oxidative stress was induced by hydrogen peroxide ($H_2O_2$) and amyloid beta 25-35 ($A{\beta}_{25-35}$), and they caused the decrease of cell viability and overproduction of reactive oxygen species (ROS). However, the treatment of protocatechuic acid significantly elevated the decreased cell viability and inhibited the overproduction of ROS by $H_2O_2$. In addition, protocatechuic acid significantly recovered the cellular damage induced by $A{\beta}_{25-35}$. In particular, protocatechuic acid at the concentration $10{\mu}g/mL$ decreased the elevated ROS level to normal level. These results indicate that protocatechuic acid may have neuroprotective effect through attenuating oxidative stress.

Ultramicroscopical Study on the Astrocytes in Fetal and Neonatal Brains of Korean Native Goat (한국재래산양태아 및 신생아 뇌에서 별아교세포의 전자현미경적 연구)

  • Song, Chi-Won;Kim, Moo-Kang;Ryu, Si-Yoon;Lee, Kang-Lee;Park, Il-Kwon;Lee, Mi-Young;Kwon, Hyo-Jung;Park, Mi-Sun;Lee, Kyoung-Youl;Lee, Doo-Hwan;Shin, Hyun-Guk;Choi, Yoon-Suk;Chang, Kyu-Tae
    • Applied Microscopy
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    • v.31 no.2
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    • pp.167-173
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    • 2001
  • This study, the ultrastructure of radial glial cells in the fetuses (the 60th, 90th, 105th 120th of gestation) and neonate brains of korean native goat were investigated by immunohistochemical method and transmisson electron microscopy. 1. In the 60th day of gestation, mitochondria and many glycogen body were observed in the radial glial cells. 2. In the 90th day of gestation, mitochondria, many glycogen body and rough endoplasmic reticulum were observed. 3. In the 95th day of gestation, Golgi's apparatus was found. 4. In the 120th day of gestation, Endfeets of radial glial cell attached vessel wall were observed.

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Apoptotic Cell Death Following Traumatic Injury to the Central Nervous System

  • Springer, Joe E.
    • BMB Reports
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    • v.35 no.1
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    • pp.94-105
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    • 2002
  • Apoptotic cell death is a fundamental and highly regulated biological process in which a cell is instructed to actively participate in its own demise. This process of cellular suicide is activated by developmental and environmental cues and normally plays an essential role in eliminating superfluous, damaged, and senescent cells of many tissue types. In recent years, a number of experimental studies have provided evidence of widespread neuronal and glial apoptosis following injury to the central nervous system (CNS). These studies indicate that injury-induced apoptosis can be detected from hours to days following injury and may contribute to neurological dysfunction. Given these findings, understanding the biochemical signaling events controlling apoptosis is a first step towards developing therapeutic agents that target this cell death process. This review will focus on molecular cell death pathways that are responsible for generating the apoptotic phenotype. It will also summarize what is currently known about the apoptotic signals that are activated in the injured CNS, and what potential strategies might be pursued to reduce this cell death process as a means to promote functional recovery.

The Role of Glial Cells in Regenerative Responses of the Injured Corticospinal Tract Axons in Rats Treated with Cindii Rhizoma (흰쥐의 척수손상 후 천궁처리에 의한 피질척수로 축삭재생 반응시 Glial cells의 역할)

  • Han, Yeong-Su;Oh, Min-Seok
    • Journal of Korean Medicine Rehabilitation
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    • v.18 no.3
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    • pp.19-39
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    • 2008
  • Objectives : It has been reported that CG was effective in decreasing injury to neural tissues. To investigate neural responses in the injured spinal cord, an extract of CG was examined to determine its effect on neural responses in the injured spinal cords of rats. Methods : After CG treatment was applied to the spinal cord of rats given a contusion injury, the re-growth responses of injured neural tissues and corticospinal tract axons was observed by measuring the number of GAP-43, Cdc2, and phospho-Erk1/2 proteins, CST axons, GFAP-stained astrocytes, and Glial scarring in the injured spinal cord. Results : Levels of GAP-43, Cdc2, and phospho-Erk1/2 proteins were found to have increased in the injured spinal cord region. The number of GFAP-stained astrocytes also increased within and around the injury cavity. Glial scarring, which was identified by CSPG immunofluorescence staining, was reduced by CG treatment. Anterograde tracing by Dil dye showed that the elongation of the CST axons in the dorso-medial white matter area was almost completely prevented at the injury site. Collateral sprouting was observed in the spinal cord rostrally close to the injury site, and CG treatment further increased axonal arborization in the corresponding region. In vivo migration of CST axons and astrocytes using an implanted polymer tube system showed more of an increase in enhanced migration of axons and astrocytes in CG-treated group compared to the injury control group. Conclusions : These results suggest that CG activated neural responses - including astrocyte migration - and promotes axonal regenerative activity in the injured spinal cord area.

The Effect of Ginseng Radix on Regeneration After Central Nervous System Injury (인삼(人蔘)이 중추신경계 손상 동물 모델의 재생에 미치는 영향)

  • Mun, Hyung-Cheal;Kim, Yun-Uk;Song, Bong-Keun
    • Journal of Acupuncture Research
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    • v.24 no.6
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    • pp.137-148
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    • 2007
  • Objectives : Following central nervous system (CNS) injury, inhibitory influences at the site of axonal damage occur. Glial cells become reactive and form a glial scar, know as gliosis. As well,myelin debris such as MAG inhibits axonal regeneration. Astrocyte-rich gliosis relates to up-regulation of GFAP and CD81, and eventually becomes a physical and mechanical barrier to axonal regeneration. It is postulated that when the astrocytic reaction is absent, regeneration of axons can occur. It was reported that treatment with anti CD81 antibodies enhanced functional recovery in rats with spinal cord injury. Methods : MAG is one of several endogenous axon regeneration inhibitors that limit recovery from central nervous system injury and disease. It was reported that molecules which block such inhibitors enhanced axon regeneration and functional recovery. Results : In this current study, the author investigated the effect of the water extract of Ginseng Radix on the regulation of CD81, GFAP and MAG which increases when gliosis occurs. MTT analysis was performed to examine cell viability, and cell based ELISA, Western Blot and PCR were used to detect the expression of CD81, GFAP and MAG. Immunohistochemistry was also performed to confirm in vivo. Conclusions : We observed that Ginseng Radix significantly down-regulates the expression of CD81, GFAP and MAG by means of cell based ELISA, Western Blot and PCR. In immunohistochemistry, expression of CD81, GFAP and MAG also decreased. Taken together, these results suggest that Ginseng Radix can be a candidate for regenerating CNS injury.

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The Effect of the Uncariae Ramulus et Uncus on the Regeneration Following CNS Injury (중추신경계 손상 회복에 미치는 대한 조구등의 영향)

  • Lee, Jin-Goo;Park, Hyoung-Jin;Kim, Dong-Woong;Song, Bong-Keun
    • Journal of Pharmacopuncture
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    • v.12 no.1
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    • pp.67-76
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    • 2009
  • Objective : Following central nervous system(CNS) injury, inhibitory influences at the site of axonal damage occur. Glial cells become reactive and form a glial scar, gliosis. Also myelin debris such as MAG inhibits axonal regeneration. Astrocyte-rich gliosis relates with up-regulation of GFAP and CD81, and eventually becomes physical and mechanical barrier to axonal regeneration. MAG is one of several endogenous axon regeneration inhibitors that limit recovery from CNS injury and disease. It was reported that molecules that block such inhibitors enhanced axon regeneration and functional recovery. Recently it was reported that treatment with anti-CD81 antibodies enhanced functional recovery in the rat with spinal cord injury. So in this current study, the author investigated the effect of the water extract of Uncariae Ramulus et Uncus on the regulation of CD81, GFAP and MAG that increase when gliosis occurs. Methods : MTT assay was performed to examine cell viability, and cell-based ELISA, western blot and PCR were used to detect the expression of CD81, GFAP and MAG. Then also immunohistochemistry was performed to confirm in vivo. Results : Water extract of Uncariae Ramulus et Uncus showed relatively high cell viability at the concentration of 0.05%, 0.1% and 0.5%. The expression of CD81, GFAP and MAG in astrocytes was decreased after the administration of Uncariae Ramulus et Uncus water extract. These results was confirmed in the brain sections following cortical stab injury by immunohistochemistry. Conclusion : The authors observed that Uncariae Ramulus et Uncus significantly down-regulates the expression of CD81, GFAP and MAG. These results suggest that Uncariae Ramulus et Uncus can be a candidate to regenerate CNS injury.