• 동의생리병리학회지
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• 제16권6호
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• pp.1134-1137
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• 2002

To investigate the neurotoxic effect of organic chloride on cultured mouse cerebral neurons, cytotoxic effect was measured by MTT assay after cultured cerebral neurons were incubated with various concentrations of methyl mercuric chloride(MMC) for 24 hours. The protective effect of Radix Polygoni Multiflori(RPM) on MMC-induced neurotoxicity was also examined in these cultures. MMC decreased cell viability of cultured mouse cerebral neurons remarkably in a dose- and time-dependent manners. In protective effect of RPM it was remarkably effective in blocking the neuroxicity induced by MMC. From aboved the results, it is suggested that MMC induce neurotoxicity, and the herba extract, RPM is very effective in preventing MMC-induced cytotoxicity on cultured mouse cerebral neurons.

• 동의생리병리학회지
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• 제17권2호
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• pp.499-502
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• 2003

Neurotoxicity of reactive oxygen species(ROS) and neuroprotective effect of Aconiti Radix(AR) against ROS-induced cytotoxicity were determined on cultured mouse cerebral neurons by MTT assay after cerebral neurons were cultured for 5 hours in various concentrations of GO. GO was toxic in a dose-dependent manner on cultured cerebral neurons after cerebral neurons were incubated for 5 hours in media containing 5～40mU/ml GO. While, cultures were pretreated with 180 μg/ml AR for 2 hours increased remarkably cell viability. From these results, it is suggested that GO has toxic effect on cultured mouse cerebral neurons by the decrease of cell viability. And also, herb extract such as AKR is very effective in the protection pf neurotoxicity induced by GO.

• 동의생리병리학회지
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• 제17권1호
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• pp.101-104
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• 2003

It has been suggested that oxidative stress of reactive oxygen species(ROS) may play a key role in the pathogenesis of neuronal complications. The aim of this study was to examine the cytotoxic effect of hydrogen peroxide(H₂O₂) in the cultured mouse cerebral neurons and the protective effect of Schisandrae Fructus(SF) on ROS-induced neurotoxicity. Cytotoxic effect of H₂O₂ and neuroprotective effect of SF were determined by MTT assay. H₂O₂ decreased cell viability in dose-and time-dependent mannner, and SF decreased H₂O₂-induced neurotoxicity in these cultures. From above the results, H₂O₂ has toxic effect, and herb extract, SF is very effective against H₂O₂-induced neurotoxicity in cultured cerebral neurons of mouse.

• 동의생리병리학회지
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• 제16권5호
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• pp.928-931
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• 2002

To elucidate the toxic effect of oxygen free radicals on cultured mouse cerebral neurons damaged by hydrogen peroxide(H₂O₂)-induced neurotoxicity, we examined the neurotoxicity induced by oxygen radicals by NR assay when cultured cerebral neurons were grown in the media containing various concentrations of H202 for 6 hours. In addition, neuroprotective effects of herb extracts such Rhizoma Gastrodiae(RG) on H202-induced neurotoxicity in cultured cerebral neurons were evaluated after cultured cerebral neurons were preincubated with various concentrations of herb extract, RG for 2 hours before 50uM H₂O₂ for 6 hours. H₂O₂ decreased remarkably cell viability in dose-and time-dependent manner in these cultures, and also herb exract, RG decreased LDH activity of cerebral neurons damaged by H₂O₂. From the above results, it is suggested that H₂O₂ was toxic in cultured cerebral neurons from mouse, and RG was effective in blocking the neurotoxicity induced by oxygen radicals in these cultures.

• 동의생리병리학회지
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• 제16권5호
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• pp.1016-1019
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• 2002

To examine the cytotoxic effect of glucose oxidase(GO) in cultured mouse cerebral neurons, cytotoxicity was measured by MTT assay after cultured nerve cells were incubated for 3 hours in the media containing 1 ～ 60mU/ml concentrations of GO. In addition, the neuroprotective effect of Ramulus et uncus uncariae(REUU) was determined by MTT assay in these cultrures. Cell viability was remarkably decreased in a dose- and time-dependent manner after cultured mouse cerebral neurons were exposed to 30mU/ml GO for 3 hours. In the neuroprotective effect of REUU on GO-induced toxicity, REUU blocked the GO-mediated neurotoxicity in these cultures. From above the results, it suggests that GO is toxic in cultured mouse cerebral neurons and selective herb extract such as REUU is effective in prevetion of the neurotoxicity induced by GO.

• 동의생리병리학회지
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• 제16권3호
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• pp.584-587
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• 2002

It has been suggested that oxidative stress may play an important role in the pathogenesis of diabetic complications. The purpose of this study was to examine the oxidative stress of streptozotocin(STZ) in the cultured mouse cerebral neurons and the preventing effect of vitamin E and and Benincasae Semen(BS) on STZ-induced neurotoxicity. Cytotoxic effect of STZ and neuroprotective effect of antioxidant and BS were performed by MTT assay. 30 μM STZ decreased cell viability in dose-and time-dependent mannner, and vitamin E and BS diminished STZ-induced neurotoxicity in these cultures. From above the results, STZ has toxic effect. and antioxidants, vitamin E or herb extract of BS is very effective against STZ-induced neurotoxicity in cultured cerebral neurons of neonatal mouse.

• 동의생리병리학회지
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• 제17권4호
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• pp.1082-1091
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• 2003

To elucidate the neuroprotective effect of Kamijihwang-hwan(KSH) on nerve cells damaged by hypoxia, the cytotoxic effects of exposure to hypoxia were determined by XTT, NR, MTT and SRB asssay. The activity of catalase and SOD was measured by spectrophometry, and TNF-α and PKC activity was measured after exposure to hypoxia and treatment of Kamijihwang-hwan(KSH) water extract(KJHWE). Also the neuroprotective effect of KJHWE was researched for the elucidation of neuroprotective mechanism. The results were as follows ; Hypoxia decreased cell viability measured by XTT, NR assay when cultured cerebral neurons were exposed to 95% N2/5% CO₂ for 2～26 minutes in these cultures and KJHWE inhibited the decrease of cell viability. H₂O₂ treatment decreased cell viability measured by MTT, and SRB assay when cultured cerebral neurons were exposed to 1-80 uM for 6 hours, but KJHWE inhibited the decrease of cell viability. Hypoxia decreased catalase and SOD activity, and also TNF-α and PKC activity in these cultured cerebral neurons, but KJHWE inhibited the decrease of the catalase and SOD activity in these cultures. Hypoxia triggered the apoptosis via caspase activation and internucleosomal DNA fragmentation. Also hypoxia stimulate the release of cytochrome c form mitochondria. KJHWE inhibited the apoptosis via caspase activation induced by hypoxia. From these results, it can be suggested that brain ischemia model induced hypoxia showed neurotoxity on cultured mouse cerebral neurons, and the KJHWE has the neuroprotective effect in blocking the neurotoxity induced by hypoxia in cultured mouse cerebral neurons.

• 한국독성학회:학술대회논문집
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• 한국독성학회 2002년도 Current Trends in Toxicological Sciences
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• pp.89-89
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• 2002

It is well known that oxygen radicals induce neuronal cell damage by initiation of lipid peroxidation chain reaction. Recent work has been also demonstrated that enzymatically generated free radicals cause the release of glutamate and aspartate from cultured rat hippocampal slices.(omitted)

• 동의생리병리학회지
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• 제19권4호
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• pp.1022-1026
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• 2005

To clarify the toxic effect on cultured neonatal mouse cerebral neurons damaged by ischemia, we examined the cytotoxicity induced by ischemia and the protective effect of antioxidant and AMPA/kainate receptor antagonist against ischemia-induced cytotoxicity on cultured cerebral neurons. For this study, mice were administrated with 20ug/kg cyclothiazide or 50U/kg vitamin E via intraperitoneal injection for 2 hours before ischemic induction. After cell culture for 7 days, cell viability, amount of neurofilament and protein kinase C activity were examined. Ischemia decreased significantly cell viability, amount of neurofilament and the increase of protein kinase C activity in these cultures. In the protective effect, vitamin I showed remarkably the increase of cell viability and amount of neurofilament, and the decrease of protein kinase C activity but, cyclothiazide did not showed any protective effect on ischemia-induced cytotoxicity. From these results, it is suggested that vitamin I is effective in blocking the neurotoxicity induced by ischemia, but cyclothiazide as a AMPA/kainate receptor antagonist is not.

• 한국한의학연구원논문집
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• 제4권1호통권4호
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• pp.99-114
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• 1998

The effect of herbal medicine on glutamate mediated neurotoxicity was studied in mouse neurons in primary culture. Immature cerebral cortex neurons (ED14) were maintained for up to 2 weeks in vitro, and we investigated the expression pattern of neuron differentiation and cytotoxicity of cell death, including LDH activity. Neuronal maturation initiated on day 7 and the susceptibility to glutamate-induced cell death was highly sensitive on Day 11 (Fig. 1). Thus, the exposure of the neurons to glutamate caused a dose$(0.1mM{\sim}1mM)$ and time$(4h{\sim}24h)$-dependent neurotoxicity(Fig. 4). Glutamate-induced neurodegeneration was prevented by Shipchondaebotang(SD), Yollyounggobondan(YG), Yugmijihwangwon(YJ) and the death of neurons exposed to glutamate was blocked by the NMDA receptor antagonist MK-801 (Fig. 5).