• 동국한의학연구소논문집
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• 제7권2호
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• pp.149-154
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• 1999

생쥐의 전뇌허혈(全腦虛血) 모델에서 potassium cyanide 유발(誘發) 혼수시간(昏睡時間) 및 생존시간(生存時間), 감압성(減壓性) 무효소(無酵素) 부하시(負荷時) 생존시간(生存時間)을 측정(測定)하여 전뇌처혈시(全腦處血時) 뇌순환대사(腦循環代謝) 개선(改善) 효과(效果)를 관찰(觀察)하였다. KCN 유발(誘發) 혼수시간(昏睡時間)의 단축(短縮), 치사양(致死量)의 KCN에 대한 생존시간(生存時間)의 연장(延長), 감압(減壓)에 의한 무산소(無酸素) 부하시(負荷時) 생존시간(生存時間)의 연장(延長) 효과(效果)가 나타났다.

• 동국한의학연구소논문집
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• 제8권1호
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• pp.171-190
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• 1999

본 실험은 전갈 추출물이 어혈병태 모델과 KCN으로 유발된 전뇌허혈, 뇌세포독성 등에 미치는 영향을 관찰하였다. 전갈은 Dextran에 의해 유도된 혈전으로 감소된 혈소판수, fibrinogen량, hemocrit치를 유의성 있게 증가시키고, 증가된 prothrombin time을 유의성 있게 단축시켰다. 전갈은 thrombin과 ADP에 의해 유도된 혈소판 응집을 억제하였으나 collagen에 의해 유도된 혈소판 응집에는 저해효과를 나타내지 않았다. 또한 collagen과 epinephrine에 의해 유도된 pulmonary embolism에 대하여 보호 효과를 나타내었다. 전갈은 KCN에 의한 전뇌허혈 유발 실험에서 혼수시간을 유의성 있게 단축시켰고, Amyloid ${\beta}$ protein(25-35)에 의해 유도된 PC12 세포의 독성에 대하여 보호효과를 나타내었다.

• 대한한의학회지
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• 제16권2호
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• pp.299-311
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• 1995

The studies were investigated in the coma time and the survival time induced by KCN, the duration of breathing after decapitation, the survival time following ligation of both common carotid arteries and the survival time after it is treated for normobaric bypoxia with a nitrogen gas, a carbon dioxide gas or a vaccum in mice. The results were as follows: 1. In histotoxic anoxia, Moschus(0.4mg／kg, p.o) demonstrated a protective effect on coma induced by a sublethal dose of KCN(1.8mg／kg, i.v.) in mice. 2. Mice subjected to a lethal dose of KCN(3.0mg／kg, i.v.) did not die by administration of Moschus. 3. Moschus was significantly extended the duration of breathing after decapitation in mice. 4. Moschus showed a significant extension of survival time in mice following ligation of both common carotid arteries. 5. In the normobaric hypoxia with a nitrogen gas, Moschus showed a significant extension of survival time in mice. 6. In the normobaric hypoxia with a carbon dioxide gas, Moschus showed a significant shortness of survival time in mice. 7. In the normobaric hypoxia with a vaccum, Moschus showed a significant extension of survival time in mice. From the above results, it is suggested that Moschus demonstrated protective effects on the brain damages induced by cerebral anoxia.

• 생약학회지
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• 제31권4호
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• pp.373-382
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• 2000

This study was performed to investigate the antithrombotic activity and protective effect of hexane fraction of Kamihyulbuchukeotang (KHCTH) on brain injury by KCN and MCA occlusion a prescription of HCT added with Lumbricus and Notoginseng Radix. Experiemental parameters are brain ischemia by MCA occlusion assay, KCN-induced brain injury, pulmonary thrombosis and platelet aggregation assay. The results were summarized as follows; 1. KHCTH extracts significantly inhibited the duration of KCN-induced coma (67%) and mortality (80%). 2. KHCTH extracts significantly suppressed brain ischemic area and edema following MCA occlusion and protected neuron cells as compared with control data. 3. KHCTH extracts inhibited pulmonary thrombosis induced by collagen and epinephrine. 4. KHCTH extracts inhibited platelet aggregation induced by collagen, ADP as agonist up to 76.9% and 32.3% respectivey at 1 mg/ml more effective than water extract of KHCT These data suggested that KHCTH could be applied as the protector of brain ischemia and injury and antithrombotic agent.

• 대한한의학회지
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• 제20권1호
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• pp.161-171
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• 1999

This study was performed to investigate the effect of complex formula(CKRG) consisting of Panax ginseng Radix rubra Koreana. Ganoderma, Cinnamomi Cortex, Glycyrrhizae Radix and Laminariae Thallus on brain ischemia and injury such as KCN-induced brain injury, forced brain ischemia, pulmonary thrombosis. The results were summarized as follows: 1. CKRG extracts showed a decrease of the duration of KCN-induced coma and showcd an increase in life expectancy. 2. CKRG extracts showed a decrease of neurologic grade in hind limb but did not affect neurologic grades in fore limb. Also. CKRG extracts showed a significant decrease of brain ischemic area and edema in MCA occlusion, 3. CKRG extracts showed a protective effect on pulmonary thrombosis induced by collagen and epinephrine. These data suggested that CKRG extracts could be applied to the protection of brain ischemia and injury.

• 혜화의학회지
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• 제8권1호
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• pp.379-401
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• 1999

The effect of KamiTongJonHaaATang extracts on hypercholesterolemia, platelet aggregation, pulm onary thrombosis, KCN-induced coma, forcal brain ischemia, cytotoxicity of PC12 cells induced by amyloid ${\beta}$ protein(25-35), and NO production in RAW cells stimulated lipopolysaccharide were investigated, respectively. The results were summarized as follows; 1. KTJHAT extracts showed a significant decrease of serum total cholesterol, triglyceride, phospholipid, LDL-cholesterol, and VLDL-cholesterol in hypercholesterolemia induced by 2% cholesterol diet in NZW rabbit. 2. KTJHAT extracts induced a significant inhibition of human platelet aggregation induced by thrombin and ADP but did not affect human platelet aggregation induced by collagen. 3. KTJHAT extracts showed a protective effect on pulmonary thrombosis induced by collagen and epinephrine. 4. KTJHAT extracts prolonged the duration of KCN-induced coma. 5. KTJHAT extracts showed a significant decrease of brain ischemic area and edema in MCA occlusion. Also, KTJHAT extracts showed a decrease of neurologic grade in hind limb but did not affect neurologic grade in fore limb. 6. KTJHAT extracts showed a protective effect on cytotoxicity of PC 12 cells induced by amyloid ${\beta}$ protein(25-35) in a dose dependent manner. 7. KTJHAT extracts showed a significant decrease of NO production in RAW cells induced by lipopolysaccharide. These results suggested that KTJHAT extracts might be usefully applied for prevention and treatement of thrombosis and brain damage.

• 대한한방내과학회지
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• 제22권4호
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• pp.503-512
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• 2001

Objective : This study was carried out to investigate the effects of DDT on the brain damage and hypertension. Methods : We observed the effect of Dodamtang(DDT) extract on KCN-induced coma, focal brain ischemia by MCA occlusion, cytotoxicity and protection of PC12 cells and B103 cells induced by amyloid ${\beta}$ protein(25-35). To prove the effect of DDT as a blood pressure depressant, we measured aldosterone, renin activity, catecholamine, sodium and NO density using the seperated blood plasma. Results : DDT showed a protective effect on cytotoxicity of PC12 cells and B103 cells induced by amyloid ${\beta}$ protein(25-35) in a dose dependent manner and proved the significant abridgement of brain ischemic area and edema induced by MCA occlusion, a critical decrease of neurologic deficitic grade in the fore-limbs. DDT didn't reduce the duration of KCN(1.87mg/kg iv.)-induced coma and prolonged the survival rate in the case of KCN(3.0mg/kg iv.)-induced coma by the ratio of 20%. While DDT increased the value of NO in SHR, it significantly decreased the blood pressure of SHR and the value of aldosterone& epinephrine in SHR. Conclusions : These results suggested that DDT might be usefully applied for treatment of hypertension, cerebral infarction, and brain damage.

• 혜화의학회지
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• 제8권1호
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• pp.425-449
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• 1999

For the evaluation of the effect on SWS, experiments were made on hyperlipidemia induced by hypercholesterol diet, inhibitory reaction to human platelet aggregation, Pulmonary thrombosis induced by collagen and epinephrine, global cerebral ischemia induced by KCN, brain ischemia induced by MCA occlusion, cytotoxicity of PC12 cells induced by amyloid ${\beta}$ protein(25-35), and NO production in RAW cells stimulated by lipopolysaccharide. The results were obtained as follows : 1. In the experiment on hyperlipidemia, the level of serum total cholesterol, phospholipid, and LDL-cholesterol were significantly decreased while the level of triglyceride, VLDL-cholesterol, and HDL-cholesterol had no significant change. 2. In the experiment on inhibitory reaction to platelet aggregation, SWS inhibited platelet aggregation induced by ADP(36.05%), by collagen(20.4%), and by thrombin(0.6%). 3. In the experiment on pulmonary thrombosis induced by collagen and epinephrine, the protective effect was found(37%). 4. In the experiment on global cerebral ischemia, coma duration induced by KCN changed insignificantly. 5. In the experiment on MCA occlusion, the change of neurologic grades on hind limb was significant only after the operation. Besides brain ischemic area and edema ratio were significantly decreased. 6. In the experiment on cytotoxicity of PC 12 cells induced by amyloid ${\beta}$ protein, the significant protective effect was found as concentration increases. 7. In the experiment on NO production in RAW cells stimulated by lipopolysaccharide, NO was significantly decreased. According to the results, it is expected that SWS might be effective on hyperlipidemia and brain damage.

• 동의생리병리학회지
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• 제18권2호
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• pp.586-595
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• 2004

Kamidojuk-San (KDJS) is known to be effective for treating cardiovascular diseases such hypertension, and clinically applied for the treatment of cerebral palsy or stoke patients. Yet, the overall mechanisms underlying its activity at the cellular levels are not known. Using experimental animal system, we investigated whether KDJS has protective effects on cells in cardiovascular and nervous systems. KDJS was found to rescue death of cultured primary neurons induced by AMPA, NMDA and kainate as well as BSO and Fe/sup 2+/ treatments. Moreover, KDJS treatment promoted animal's recovery from coma induced by a lethal dose of KCN treatment, and improved survival in animals exposed to lethal dose of KCN. Neurological examinations further showed that KDJS reduced the time which is required for animals to respond in terms of forelimb and hindlimb movements. To examine its physiological effects on cardiovascular and nervous systems, we induced ischemic injury in hippocampal neurons and cerebral neurons by middle cerebral artery (MCA) occlusion. Histological examination revealed that KDJS significantly protected neurons from ischemic damage. Thus, the present data suggest that KDJS may play an important role in protecting cells of cardiovascular and nervous systems from external noxious stimulations.

• 동의생리병리학회지
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• 제18권1호
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• pp.265-273
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• 2004

KBPTS is the fortified prescription of Bang-pung-tong-sung-san (BPTS) by adding Spatholobi Clulis and Salviae Miltiorrzae Radix. BPTS prescription has been used in Qriental medicine for the treatments of vascular diseases including hypertension, stroke, and arteriosclerosis, and nervous system diseases. Yet, the overall mechanism underlying its activity at the cellular levels remains unknown. To investigate the protective role of KBPTS on brain functions, noxious stimulations were applied to neurons in vitro and in vivo. KBPTS pretreatment in cultured cortical neurons of albino ICR mice rescued death caused by AMPA, NMDA, and kainate as well as by buthionine sulfoximine (BSO) and ferrous chloride (Fe/sup 2+/) treatments. Furthermore, KBPTS promoted animal's recovery from coma induced by a sublethal dose of KCN and improved survival by a lethal dose of KCN. To examine its physiological effects on the nervous system, we induced ischemia in the Sprague-Dawley rat's brain by middle cerebral artery (MCA) occlusion. Neurological examination showed that KBPTS reduced the time which is required for the animal after MCA occlusion to respond in terms of forelimb and hindlimb movement$. Histological examination revealed that KBPTS reduced ischemic area and edema rate and also protected neurons in the cerebral cortex and hippocampus from ischemic damage. Thus, the present data suggest that KBPTS may play an important role in protecting neuronal cells from external noxious stimulations.