• 제목/요약/키워드: glial cells

검색결과 278건 처리시간 0.025초

Methanol이 배양된 흰쥐 해마의 신경세포 및 신경교 세포의 성장에 미치는 영향 (Effect of Methanol on Cultured Neuronal and Glial Cells on Rat Hippocampus)

  • 이정임;조병채;배영숙;이경은
    • Toxicological Research
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    • 제12권2호
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    • pp.203-211
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    • 1996
  • Methanol has been widely used as an industrial solvent and environmental exposure to methanol would be expected to be increasing. In humans, methanol causes metabolic acidosis and damage to ocular system, and can lead to death in severe and untreated case. Clinical symptoms are attributed to accumulation of forrnic acid which is a metabolic product of methanol. In humans and primates, formic acid is accumulated after methanol intake but not in rodents due to the rapid metabolism of methanol. Neverthless, the developmental and reproductive toxicity were reported in rodents. Previous reports showed that perinatal exposure to ethanol produces a variety of damage in human central nervous system by direct neurotoxicity. This suggests that the mechanism of toxic symptoms by methanol in rodents might mimic that of ethanol in human. In the present study I hypothesized that methanol can also induce toxicity in neuronal cells. For the study, primary culture of rat hippocampal neurons and glias were empolyed. Hippocampal cells were prepared from the embryonic day-17 fetuses and maintained up to 7 days. Effect of methanol (10, 100, 500 and 1000 mM) on neurite outgrowth and cell viability was investigated at 0, 18 and 24 hours following methanol treatment. To study the changes in proliferation of glial cells, protein content was measured at 7 days. Neuronal cell viability in culture was not altered during 0-24 hours after methanol treatment. 10 and 100 mM methanol treatment significantly enhanced neurite outgrowth between 18-24 hours. 7-day exposure to 10 or 100 mM methanol significantly increased protein contents but that to 1000 mM methanol decreased in culture. In conclusion, methanol may have a variety of effects on growing and differentiation of neurons and glial cells in hippocampus. Treatment with low concentration of methanol caused that neurite outgrowth was enhanced during 18-24 hours and the numbers of glial cell were increased for 7 days. High concentration of methanol brought about decreased protein contents. At present, the mechanism responsible for the methanol- induced enhancement of neurite outgrowth is not clear. Further studies are required to delineate the mechanism possibly by employing molecular biological techniques.

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면역조직화학적 방법을 이용한 흰쥐의 호모시스테인 수준과 망막 손상의 관련성 연구 (Effects of Hyperhomocysteinemia on the Immunohistochemical Reactivity for Vimentin in the Retinal Glial Cell)

  • 이인선;이화영;장남수
    • Journal of Nutrition and Health
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    • 제38권2호
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    • pp.96-103
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    • 2005
  • It has been suggested that the elevated plasma homocysteine may lead to retinal dysfunction. We investigated the effects of plasma levels of homocysteine and folate on the retinal glial cells' injuries. Male Sprague-Dawley rats were raised either on a control diet or on an experimental diet containing 3.0 g/kg homocystine without folic acid for 10 weeks. Plasma homocysteine concentrations were measured by a HPLC-fluorescence detection method. Plasma folate and vitamin B/sub 12/ levels were analyzed by a radioimmunoassay. The response of Muller cells which are the principal glial cells of the retina was immunohistochemically examined using an antibody for vimentin, a cytoskeletal protein belonging to the family of intermediate filament. At 2 weeks, the homocystine diet induced a twofold increase in plasma homocysteine, and a concomitant increase in the expression of vimentin in the Muller cells' processes spanning from the inner to outer membranes of the retina indicating arterial degeneration. At 10 weeks, the homocystine diet induced a fourfold increase in plasma homocystine, but vimentin immunoreactivity in the retinas was similar in both groups. In conclusion, increased plasma homocysteine levels have influence on morphological and functional changes of Muller cells in the retina. (Korean J Nutrition 38(2): 96~103, 2005)

Protective role of paeoniflorin from hydrogen peroxide-mediated oxidative damage in C6 glial cells

  • Lee, Ah Young;Nam, Mi Na;Kim, Hyun Young;Cho, Eun Ju
    • Journal of Applied Biological Chemistry
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    • 제63권2호
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    • pp.137-145
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    • 2020
  • Oxidative stress is one of the pathogenic mechanisms of various neurodegenerative diseases, such as Alzheimer's disease. Neuroglia, the most abundant cells in the brain, is thought to play an important role in the antioxidant defense system and neuronal metabolic support against neurotoxicity and oxidative stress. We investigated the protective effect of paeoniflorin (PF) against oxidative stress in C6 glial cells. Exposure of C6 glial cells to hydrogen peroxide (H2O2, 500 μM) significantly decreased cell viability and increased amounts of lactate dehydrogenase (LDH) release, indicating H2O2-induced cellular damage. However, treatment with PF significantly attenuated H2O2-induced cell death as shown by increased cell survival and decreased LDH release. The H2O2-stimulated reactive oxygen species production was also suppressed, and it may be associated with improvement of superoxide dismutase activity by treatment with PF. In addition, an increase in ratio of Bcl-2/Bax protein expression was observed after treatment with PF. In particular, the down-stream of the apoptotic signaling pathway was inhibited in the presence of PF, mostly by reduction of cleaved-poly ADP ribose polymerase, cleaved caspase-3, and -9 protein expression. Furthermore, H2O2-induced phosphorylation of c-Jun N-terminal kinase and extracellular signal-regulated kinase 1/2 was attenuated by treatment with PF. Taken together, neuroprotective effect of PF against oxidative stress probably result from the regulation of apoptotic pathway in C6 glial cells. In conclusion, our findings suggest that PF may be a potent therapeutic agent for neurodegenerative disorders.

Caffeic Acid의 항산화 활성 및 Amyloid beta와 LPS에 의한 C6 Glial 세포의 산화적 스트레스 보호 효과 (Antioxidant Activity and Protective Effect of Caffeic Acid against Oxidative Stress Induced by Amyloid Beta and LPS in C6 Glial Cells)

  • 김지현;왕천;이상현;조은주
    • 생약학회지
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    • 제46권2호
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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.

흰쥐의 소뇌에서 selenium 방법에 의한 아연이 함유된 세포의 확인 (Identification of the Zinc-containing Cells in the Cerebellum of Rat by Selenium Method)

  • 조현욱;최은상
    • Applied Microscopy
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    • 제26권4호
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    • pp.411-420
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    • 1996
  • A zinc-specific method (selenium method) has been employed to identify the zinc-containing cells in the cerebellum of the rats. When rats were allowed to survive 24 hours after the sodium selenite administration, zinc selenide reaction products formed in zinc-containing cellular boutons are retrogradely transported to the somata of those boutons. And the zinc selenide products accumulated in somata of the cells can be rendered visible by silver amplification of developer. Zinc-containing cells identified by the method were Bergmann glial and granule cells. Labeled zinc-containing cells were absent in molecular layer and white matter of the cerebellum. In ultrastructural level, the zinc selenide products were located in lysosomes of somata of the zinc-containing cells.

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종류별 감초의 라디칼 소거능 및 H2O2에 의한 C6 glial 세포의 산화적 스트레스 개선 효과 (Free radical scavenging activity and protective effect of three glycyrrhiza varieties against hydrogen peroxide-induced oxidative stress in C6 glial cells)

  • 김지현;조민지;박찬흠;조은주;김현영
    • Journal of Applied Biological Chemistry
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    • 제63권4호
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    • pp.327-334
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    • 2020
  • 산화적 스트레스는 신경퇴행성 질환 발병의 원인으로 알려져 있다. 본 연구는 대표적인 감초 종류인 Glycyrrhiza glabra, G. uralensis와 신품종 감초인 신원감(SW)의 in vitro free radical 소거능을 통한 항산화 활성과 H2O2 유도 산화적 스트레스에 대한 C6 glial cell 보호 효능을 확인하고자 하였다. In vitro assay에서 G. uralensis, G. glabra, SW 추출물은 농도유의적으로 2,2-diphenyl-1-picrylhydrazyl, ·OH, O2- radical 소거능이 증가하여 in vitro 항산화 활성을 확인하였다. 또한, SW 추출물은 G. uralensis, G. glabra 추출물에 비해 총 페놀 및 플라보노이드 함량이 가장 우수하였다. H2O2로 산화적 스트레스를 유도한 C6 glial cell에 3가지 감초 추출물을 각각 처리 시, 농도의존적으로 세포 생존율이 증가와 reactive oxygen species 소거능이 증가하여 3가지 감초 추출물의 산화적 손상에 대한 신경교세포 보호 효과를 확인하였다. 특히, SW 추출물은 G. uralensis, G. glabra 추출물에 비해 우수하게 C6 glial cell 보호 효과를 나타내었다. 또한, 3가지 감초 추출물의 신경교세포 보호 메커니즘을 확인하기 위해, 염증 관련 단백질 발현을 측정하였다. 3가지 감초 추출물은 H2O2만을 처리한 control군에 비해 inducible nitric oxide synthase 및 cyclooxygenase-2 발현 감소를 통해 염증반응 조절을 통한 신경교세포 보호 작용기전을 확인하였다. 본 연구는 G. uralensis, G. glabra, SW 등 3가지 감초 추출물이 산화적 손상이 유도된 신경교세포 보호에 유용한 소재로써의 가능성이 있는 것으로 사료된다.

자감초탕(炙甘草湯)이 LPS와 PMA에 의해 손상된 C6 glial 세포에 미치는 영향 (Effects of Jagamcho-tang on the C6 Glial Cell Injured by LPS Combined PMA)

  • 조남수;유준기;이인;신선호;문병순;나영훈
    • 대한한방내과학회지
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    • 제21권3호
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    • pp.467-475
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    • 2000
  • The water extracts of Jagamcho-tang has been used for treatment of arrhythmia and palpitation in oriental traditional medicine. Brain is provided with blood flow by heart. Jagamcho-tang has been studied on ischemia and infarction in heart. However, little is known about the mechanism by which the water extracts of Jagamcho-tang rescues brain cells from ischemic damages. To elucidate the protective mechanism on ischemic induced cytotoxicity, the effects of Jagamcho-tang on ischemia induced cytotoxicity and generation of nitric oxide(NO) are investigated in C6 glioma cells. Jagamcho-tang induce NO in a dose dependent manner up to 2.5mg/ml in C6 glioma cells. The pretreatment of Jagamcho-tang protect sodium nitroprusside(SNP) (2mM) induced cytotoxicity. This effect of Jagamcho-tang is mimicked by treatment by pretreatment of SNP($100{\mu}M$), an exogenous NO donor. NG-monomethyl-L-arginine($N^{G}MMA$), a specific inhibitor of nitric oxide synthase (NOS), significantly blocks the protective effects of Jagamcho-tang on cell toxicity by ischemia. In addition, lipopolysaccharide(LPS) and phorhol 12 myristate 13-acetate(PMA) treatment for 72h in C6 glial cells markedly induce NO, but treatment of the cells with the water extracts of Jagamcho-tang decrease nitrite formation in a dose dependent manner. In addition, LPS and PMA treatment for 72h induce severe cell death and LDH release into medium in C6 glial cells. However treatment of the cells with the water extracts of Jagamcho-tang dose not induce significant changes compare to control cells. Furthermore, the protective effects of the water extracts of Jagamcho-tang is mimicked by treatment of $N^{G}MMA$. Taken together, I suggest that the protective effects of the water extracts of Jagamcho-tang against ischemic brain damages may be mediated by regulation of iNOS during ischemic condition.

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신경아교세포와 기분장애 (Neuroglia and Mood Disorder)

  • 이정구;서미경;박성우;김영훈
    • 생물정신의학
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    • 제22권2호
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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.

Store-operated calcium entry in the satellite glial cells of rat sympathetic ganglia

  • Sohyun Kim;Seong Jun Kang;Huu Son Nguyen;Seong-Woo Jeong
    • The Korean Journal of Physiology and Pharmacology
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    • 제28권1호
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    • pp.93-103
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    • 2024
  • Satellite glial cells (SGCs), a major type of glial cell in the autonomic ganglia, closely envelop the cell body and even the synaptic regions of a single neuron with a very narrow gap. This structurally unique organization suggests that autonomic neurons and SGCs may communicate reciprocally. Glial Ca2+ signaling is critical for controlling neural activity. Here, for the first time we identified the machinery of store-operated Ca2+ entry (SOCE) which is critical for cellular Ca2+ homeostasis in rat sympathetic ganglia under normal and pathological states. Quantitative realtime PCR and immunostaining analyses showed that Orai1 and stromal interaction molecules 1 (STIM1) proteins are the primary components of SOCE machinery in the sympathetic ganglia. When the internal Ca2+ stores were depleted in the absence of extracellular Ca2+, the number of plasmalemmal Orai1 puncta was increased in neurons and SGCs, suggesting activation of the Ca2+ entry channels. Intracellular Ca2+ imaging revealed that SOCE was present in SGCs and neurons; however, the magnitude of SOCE was much larger in the SGCs than in the neurons. The SOCE was significantly suppressed by GSK7975A, a selective Orai1 blocker, and Pyr6, a SOCE blocker. Lipopolysaccharide (LPS) upregulated the glial fibrillary acidic protein and Toll-like receptor 4 in the sympathetic ganglia. Importantly, LPS attenuated SOCE via downregulating Orai1 and STIM1 expression. In conclusion, sympathetic SGCs functionally express the SOCE machinery, which is indispensable for intracellular Ca2+ signaling. The SOCE is highly susceptible to inflammation, which may affect sympathetic neuronal activity and thereby autonomic output.

Protective effect of Cirsium japonicum var. maackii against oxidative stress in C6 glial cells

  • Lee, Ah Young;Kim, Min Jeong;Lee, Sanghyun;Shim, Jae Suk;Cho, Eun Ju
    • 농업과학연구
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    • 제45권3호
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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.