• 사상체질의학회지
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• 제11권2호
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• pp.267-281
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• 1999

1. 연구목적 본 실험은 태음조위탕이 대뇌신경세포의 산화적 손상에 대한 효능을 밝히기 위한 것이다. 2. 연구방법 신생생쥐에서 순수 분리한 대뇌신경세포(大腦神經細胞)를 배양(培養)하여 glucose oxidase (GO)에 노출시킨 후 이의 독성효과(毒性效果)를 측정(測定)하였으며, 또한 GO에 의하여 유도(誘導)된 독성(毒性)에 대한 태음조위탕(太陰調胃湯)의 효과(效果)를 조사(調査)하였다. 3. 결과 및 결론 산소자유기(酸素自由基)인 GO는 MTTassay에 의한 세포생존율(細胞生存率)의 유의한 감소(減少)를 보였다. 산소자유기(酸素自由基)인 GO는 NR assay에 의한 세포생존율(細胞生存率)의 유의한 감소(減少)를 보였다. GO의 산화적(酸化的) 손상(損傷)에 의한 신경독성(神經毒性)에 대하여 태음조위탕(太陰調胃湯) 투여로 총단백질양의 유의한 증가(增加)를 보였다. GO의 산화적(酸化的) 손상(損傷)에 의한 신경독성(神經毒性)에 대하여 태음조위탕(太陰調胃湯) 투여로 lipid peroxidation의 유의한 감소(減少)를 보였다. 이상(以上)의 실험결과(實驗結果)는 태음조위탕(太陰調胃湯)이 대뇌신경세포(大腦神經細胞)의 산화적손상(酸化的損傷)에 대하여 유의성(有意性) 있는 방어적(防禦的) 작용(作用)을 나타낸 것으로, 이와 관련된 노화억제(老化抑制)나 뇌허혈(腦虛血), 다발성경화증(多發性硬化症), 치매 등 뇌기능손상(腦機能損傷)이나 저하(低下)로 유발되는 질환(疾患)에 대한 임상응용(臨床應用)에 대해서도 지속적(持續的)인 연구(硏究)가 필요(必要)하다고 사료(思料)된다.

• 동의생리병리학회지
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• 제17권1호
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• pp.136-139
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• 2003

Cytotoxicity of glucose oxidase(GO) and cardioprotective effect of Salviae Multiorrhizae Radix(SMR) against GO-induced cardiotoxicity were measured for evaluation of cardiotoxicity on cultured mouse pulmonary endotherial cells(PEC) by MTT assay after PEC were cultured for 8 hours at various concentrations of GO. GO was toxic in a time and dose-dependent manner on cultured PEC after PEC were grown for 8 hours in media containing 1～60mU/ml GO. While, cultures were pretreated with 60 μg/ml SMR for 2 hours increased remarkably cell viability. From the above results, it is suggested that GO is toxic on cultured PEC by the decrease of cell viability, and herb medicine such as SMR is very effective in the prevention of vascular toxicity induced by GO.

• 동의생리병리학회지
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• 제17권2호
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• pp.457-460
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• 2003

It has been suggested that oxidative stress of reactive oxygen species(ROS) may play an important role in the pathogenesis of neurological disorder. The aim of this study was to elucidate the oxidative stress of glucose oxidase(GO) in the cultured mouse spinal motor neurons and the preventing effect of Benincasae Semen(BS) on ROS-induced neurotoxicity. Cytotoxic effect of GO and protective effect of BS were performed by MTT assay. 30mU/ml GO decreased cell viability in dose-and time-dependent mannner, and BS diminished GO-induced neurotoxicity in these cultures. From above the results, ROS such as GO has toxic effect, and herb extract of BS is very effective against GO-induced neurotoxicity in cultured spinal motor neurons of neonatal mouse.

• 대한한의학방제학회지
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• 제7권1호
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• pp.143-151
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• 1999

척수감각신경절세포에 대한 산소자유기의 신경독성효과에 대한 기전을 규명하기 위하여 여러 농도의 Glucose Oxidase(GO)를 배양 척수 감각신경절세포에 처리한 후 GO의 독성효과를 분석하였으며 또한 GO에 의하여 유발된 신경독성에 대한 음양곽(Epimedium Koreanum Nakai)의 방어효과를 MTT assay법에 의하여 조사하여 다음과 같은 결론을 얻었다. GO는 신경세포에 처리한 농도와 시간에 비례하여 세포의 생존율을 유의하게 감소시켰으며, 또한 음양곽이 GO의 독성효과를 효과적으로 방어하였다. 이상의 결과로부터 산소자유기인 GO는 생쥐의 배양 척수감각신경절세포에 독성을 나타냈으며 음양곽과 같은 한약추출물이 GO의 독성을 방어하는데 효과적인 것으로 나타났다.

• 동의생리병리학회지
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• 제16권1호
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• pp.141-145
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• 2002

In order to clarify the neuroprotective effect of Gamibojungikki-tang (GBJIKT) water extract on cultured mouse spinal sensory neuron damaged by glucose Oxidase (GO), MTT [3-(4,5-dimethylthiazole-2-yl) -2,5-diphenyltetrazolium bromide] assay and SRB (Sulforhodamine B) assay were carried out after the cultured mouse spinal sensory neuron were preincubated with various concentrations of GBJIKT water extract for 3 hours prior to exposure of GO. Cell viability of cultured mouse spinal sensory neurons exposed to various concentrations of GO for 8 hours was decreased in a dose-dependent manner. MTT50 values were 45 mU/ml GO. Cultured mouse spinal sensory neurons in the medium containing various concentration of GO for 8 hours showed decreasing of total protein synthesis. GO was toxic on cultured spinal sensory neurons. Pretreatment at GBJIKT water extract for 3 hours following GO prevented the GO-induced neurotoxicity such as decreasing of total protein synthesis. These results suggest that GO shows toxic effect on cultured spinal sensory neurons and GBJIKT water extract is highly effective in proecting the neurotoxicity induced by GO.

• 동의생리병리학회지
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• 제16권3호
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• pp.495-498
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• 2002

Cytotoxicity of glucose oxidase(GO) and neuroprotective effect of Aconiti Radix(AKR) against GO-induced neurotoxicity were measured for elucidating the mechanism of cardiotoxicity on cultured mouse myocardial cells by MTT assay after myocardial cells were cultured for 24 hours at various concentrations of GO. GO was toxic in a time-and dose-dependent manner on cultured myocardial cells after myocardial cells were grown for 24 hours in media containing 5～40mU/ml GO. While, cultures were pretreated with 50 μg/ml AKR for 2 hours increased remarkably cell viability. From the above results, it is suggested that GO is toxic on cultured mouse myocardial cells by the decrease of cell viability, and herb medicine such as AKR is very effective in the prevention of myocardial toxicity induced by GO.

• 동의생리병리학회지
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• 제16권6호
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• pp.1197-1200
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• 2002

To examine the cardiotoxicity of glucose oxidase(GO) in cultured myocardial cells, cardiotoxicity was measured by MTT assay. Myocardial cells were treated with 1～50 mU/ml GO for 5 hours. The cardioprotective effect of Benincasae Semen(BS) was measured by MTT assay in these cultrures. Cell viability was significantly decreased in dose- and time-dependently after myocardial cells were exposed to 30mU/ml GO for 5 hours. In the cardioprotective effect of BS on the cardiotoxicity induced by GO, BS prevented the cardiotoxicity induced by GO in these cultures. From these results, it suggests that GO had cytotoxic effect in cultured myocardial cells and herb extract, BS showed protective effect on GO-induced cardiotoxicity.

• 한국식품과학회지
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• 제23권4호
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• pp.517-519
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• 1991

글루코오스 산화효소와 수피옥사이드 디스뮤타제가 유지의 산화를 억제할 수 있는지 여부를 알아보기 위하여 이들 효소와 기질을 어유에 직접 용해시키고 시료를 vial에 담아 저장하면서 상부공간의 산소함량과 어유의 과산화물값의 변화를 측정하였다. GO 첨가구의 경우 산소의 감소속도는 대조구와 비슷하였으나 과산화물값은 훨씬 낮은 수준이었다. 이러한 결과는 산소의 일부가 GO의 기질로 소모되어 유지의 산화에 공급된 산소가 제한되었기 때문으로 풀이된다. SOD를 첨가하였을 때에도 유지의 산화가 억제되었는데 이는 SOD가 반응성이큰 일중항 산소를 기저상태의 산소로 전환시킬 수 있었기 때문으로 생각된다.

• 동의신경정신과학회지
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• 제10권1호
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• pp.53-78
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• 1999

As the average life span have been lengthened and the rate of senile population have been raised, chronic degenerative diseases incident to aging has been increased rapidly and become a social problem. With this social background, recently, the facts that oxygen radicals(OR) have toxic effects on Central Nervous System and Peripheral Nervous System and cause neuropathy such as Parkinson's Disease, Alzheimer Disease have been turned out, and accordingly lots of studies on the mechanism of the toxic effects of OR on nerves, the diseases caused by OR and the approaches to curing the diseases have been made. The purpose of this study is to examine the toxic effects caused by Glucose Oxidase(GO) and the effects of herbal extracts such as Chilbokyeum(CBY), Chilbokyeumga Acori Rhizoma(CAR), Acori Rhizoma(AR) on the treatment of the toxic effects. For this purpose, experiments with the cultured cell from the cerebrums of new born mice were done. The results of these experiments were as follows. 1. GO, a oxygen radical, decreased the survival rate of the cultured cells on NR assay, MTT assay and amount of neurofilaments and increased the amount of total protein, lipid peroxidation and the amount of LDH. 2. CBY have efficacy of increasing the amount of neurofilaments and total protein and decreasing lipid peroxidation and the amount of LDH. 3. CAR have efficacy of increasing the amount of neurofilaments and total protein and decreasing lipid peroxidation and the amount of LDH. 4. AR have efficacy of increasing the amount of neurofilaments and total protein. From the above results, It is concluded that Chilbokyeumgamibang has marked efficacy as a treatment for the damages caused in the GO-mediated oxidative process. And Chilbokyeumgamibang is thought to have certain pharmacological effects on controlling over aging and treating Dementia. Further clinical study of this pharmacological effects of Chilbokyeumgamibang should be complemented.

• Molecules and Cells
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• 제22권1호
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• pp.21-29
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• 2006

The aim of this study was to determine if hydrogen peroxide ($H_2O_2$) generated by glucose oxidase (GO) induces apoptosis or necrosis of BJAB cells and which radical is the direct mediator of cell death. We found that GO produced $H_2O_2$ continuously in low concentrations, similar to in vivo conditions, and decreased proliferation and cell viability in a dose-dependent manner. The GO-mediated cytotoxicity resulted from apoptosis, and was confirmed by monitoring the cells after H33342/Annexin V/propidium iodide staining. Decreases of mitochondrial membrane potential and intracellular glutathione level were found to be critical events in the $H_2O_2$-mediated apoptosis. Additional experiments revealed that $H_2O_2$ exerted its apoptotic action through the formation of hydroxyl radicals via the Fenton rather than the Haber-Weiss reaction. Moreover, intracellular redox-active iron, but not copper, participated in the $H_2O_2$-mediated apoptosis.