• 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.

• 한국식품영양과학회지
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• 제35권2호
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• pp.132-138
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• 2006

혈전성 질환을 예방 및 치료할 수 있는 트롬빈 직접 저해제 개발은 전 세계적으로 지속적으로 이루어지고 있다. 본 연구에서는 안전성이 확보된 식용 및 약용식물로부터 트롬빈 직접저해제를 탐색하였으며, 그 결과 메밀 종자의 메탄올 추출물 및 주정 추출물에서 강력한 트롬빈 저해활성을 확인하였다. 메탄올 추출물의 순차적 유기 용매 분획 결과 부탄올 및 에틸아세테이트 분획물에서 가장 우수한 트롬빈 저해활성을 나타내었다. 특히 주정 추출물의 부탄올 분획의 경우 $312.5{\mu}g/mL$의 낮은 농도에서도 $2,000\%$이상의 트롬빈 저해 활성을 나타내어, 아스피린보다 매우 효율적으로 혈전 생성을 억제함을 확인하였다. 활성성분은 30 KD 이상의 고분자 비단백질 성분임을 확인하였으며, 산 및 열처리에 의해 급격한 활성 감소가 나타나, 활성 물질의 효율적인 이용을 위해서는 메밀 종자의 비열, 비산 처리공정이 필요하리라 추측되었다. 또한 활성 분획물은 ICR 마우스를 이용한 폐색전 실험, 전뇌 허혈성 실험 및 치사유발실험에서 아스피린보다 우수한 혈전성 마비 억제, 혼수방지 및 치사억제 활성을 보여, 혈행 개선제 및 항혈전제로 개발 가능함을 제시하였다.

• 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.

• 동의생리병리학회지
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• 제16권2호
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• pp.245-256
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• 2002

This studt was investigated to prove the effect of SPBST on the hypertension, the thrombosis and the brain damage. The results were as follows; 1. SPBST affected the htpertension as adepressant, but insignificant. 2. SPBST decreased significantly dopamine, aldosterone but ineffective on the epinephrine, norepinephrine and renin activity. 3. SPBST increased the NO product but insignificant. 4. SPBST had a death suppression effect by 50% in pulmonary thrombosis inducement experiment and activated slightly on the fibrinolytic activity. 5. SPBST suppressed significantly platelet diminution and prolonged insignificantly PT and APTT. 6. On the measure of the blood flow rate induced by the thrombus, in vivo SPBST accelerated the blood flow rate, in vitro insignificant. 7. SPBST had no toxicity on the PC12 cell and B103 cell induced by amyloid β protein (-35) and a protective effect, in proportion to the density. 8. SPBST decreased significantly coma duration time in a Infatal dose of KCN and showed 50% of survival rate in a fatal dose. 9. SPBST decreased significantly ischemic area and edema incited by the MCA blood flow block. These results indicate that SPBST can be used in hypertension, the thrombosis, the brain damage, the ischemic cerebral infarction and the acute stage of the brain damage. Further study will be needed about the functional mechanism and etc.

• 대한한의학회지
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• 제25권3호
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• pp.32-44
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• 2004

Objectives : This study was undertaken to prove the effect of GSHT on the glutamate receptor, free radical and brain damage in rats subjected to brain ischemia Methods : Levels of cultured cortical neuron death caused by toxic chemicals were measured by LDH release assay. Neuroprotective effects of GSHT on brain tissues were examined in vivo by ischemic model of middle cerebral artery (MCA) occlusion. Results : GSHT showed significant inhibitory effect on LDH release induced by NMDA-kinate-Fe/sup 2+/. GSHT remarkably decreased coma duration time in a nonfatal dose of KCN and showed higher survival rate in a fatal dose. GSHT remarkably decreased ischemic area and edema induced by the MCA blood flow block. GSHT showed high improvement of forelimb and hind limb test after MCA occlusion in neurological examination. GSHT showed no significant change after MCA occlusion in pathological observation of the normal group. Conclusions : These results indicate that GSHT can be used to treat the brain damage caused by brain ischemia. Further study will be needed about the functional mechanism, etc.