• 생명과학회지
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• 제30권11호
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• pp.939-946
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• 2020

뇌졸중은 전 세계적으로 신경계 장애를 일으키는 주요 원인 중 하나이며, 뇌졸중 환자는 다양한 운동, 인지 및 정신 장애를 나타낸다. GPR88은 orphan G protein coupled receptor이며 striatal medium spiny neurons에서 높게 발현이 되며, GPR88이 결손이 된 경우 motor coordination과 motor learning에 문제가 발생하게 된다. 본 연구에서는 Western blot 및 real-time PCR을 사용하여 허혈성 마우스 모델에서 GPR88 발현이 감소함을 발견 하였다. 또한, 뇌에서 유래한 세 가지 유형의 세포들, 뇌혈관내피세포(brain microvascular endothelial cells), 미세 아교세포(microglial cells) 및 신경 세포들에서 GPR88의 발현정도를 확인한 결과, HT22 신경 세포에서 GPR88의 발현이 가장 높음을 관찰하였고, 뇌졸중과 유사한 실험조건인 oxygen glucose deprivation (OGD) 조건에 배양한 HT22 신경세포에서 GPR88의 발현이 감소하였다. 또한 GPR88 효현제인 RTI-13951-33 (10 mg/kg)을 전처리후에 뇌허혈을 유발하였을 때, infarct volume의 감소, vestibular-motor function 및 neurological score의 개선효과를 관찰할 수 있었다. 이러한 결과는 GPR88이 허혈성 뇌졸중을 포함한 CNS 질환의 치료를 위한 잠재적인 약물표적이 될 수 있음을 제시한다.

• 대한한의학회지
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• 제29권5호
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• pp.29-40
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• 2008

Objectives : It has been reported that Sophorae Subprostratae Radix (SSR) has a neuroprotective effect on cerebral ischemia in animals. In the present study, the authors investigated the neuroprotective effect of SSR on glutamate excitotoxicity. Glutamate excitotoxicity was induced by using NMDA, AMPA, and KA in PC12 cells and in organotypic hippocampal slice cultures. Methods :Methanolic extract of SSR was added at 0.5, 5, and 50 ${\mu}$g/ml to culture media for 24 hours. The effects of SSR were evaluated by measuring of cell viability, PI-stained neuronal cell death, TUNEL-positive cells, and MAP-2 immunoreactivity. Results : SSR increased PC12 cell viabilities significantly against AMPA-induced excitotoxicity, but not against NMDA-induced or KA-induced excitotoxicity. In organotypic hippocampal slice cultures damaged by NMDA-induced excitotoxicity, SSR attenuated neuronal cell death significantly in the CA1, CA3, and DG hippocampal regions and reduced TUNEL-positive cells significantly in CA1 and DG regions. In organotypic hippocampal slice cultures damaged by AMPA-induced excitotoxicity, SSR attenuated neuronal cell death and reduced TUNEL-positive cell numbers significantly in the CA1 and DG regions. In organotypic hippocampal slice cultures damaged by KA-induced excitotoxicity, SSR attenuated neuronal cell death significantly in CA3, but did not reduce TUNEL-positive cell numbers in CA1, CA3 or DG. In organotypic hippocampal slice cultures damaged by NMDA-induced excitotoxicity, SSR attenuated pyramidal neuron neurite retraction and degeneration in CA1. Conclusions : These results suggest that the neuroprotective effects of SSR are related to antagonistic effects on the NMDA and AMPA receptors of neuronal cells damaged by excitotoxicity and ischemia.

• Korean Journal of Acupuncture
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• 제17권1호
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• pp.101-121
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• 2000

The purpose of this morphological studies was to investigate the relation to the meridian, acupoint and nerve. The common locations of the spinal cord and brain projecting to the the gallbladder, GB34 and common peroneal nerve were observed following injection of transsynaptic neurotropic virus, pseudorabies virus(PRV), into the gallbladder, GB34 and common peroneal nerve of the rabbit. After survival times of 96 hours following injection of PRV, the thirty rabbits were perfused, and their spinal cord and brain were frozen sectioned($30{\mu}m$). These sections were stained by PRV immunohistochemical staining method, and observed with light microscope. The results were as follows: 1. In spinal cord, PRV labeled neurons projecting to the gallbladder, GB34 and common peroneal nerve were founded in thoracic, lumbar and sacral spinal segments. Densely labeled areas of each spinal cord segment were founded in lamina V, VII, X, intermediolateral nucleus and dorsal nucleus. 2. In medulla oblongata, The PRV labeled neurons projecting to the gallbladder, GB34 and common peroneal nerve were founded in the A1 noradrenalin cells/C1 adrenalin cells/caudoventrolateral reticular nucleus, rostroventrolateral reticular nucleus, medullary reticular nucleus, dorsal motor nucleus of vagus nerve, nucleus tractus solitarius, raphe obscurus nucleus, raphe pallidus nucleus, raphe magnus nucleus, gigantocellular nucleus, lateral paragigantocellular nucleus, principal sensory trigeminal nucleus and spinal trigeminal nucleus. 3. In Pons, PRV labeled neurons were parabrachial nucleus, Kolliker-Fuse nucleus and cochlear nucleus. 4. In midbrain, PRV labeled neurons were founded in central gray matter and substantia nigra. 5. In diencephalon, PRV labeled neurons were founded in lateral hypothalamic nucleus, suprachiasmatic nucleus and paraventricular hypothalamic nucleus. 6. In cerebral cortex, PRV labeled neuron were founded in hind limb area.This results suggest that PRV labeled common areas of the spinal cord projecting to the gallbladder, GB34 and common peroneal nerve may be first-order neurons related to the somatic sensory, viscero-somatic sensory and symapathetic preganglionic neurons, and PRV labeled common area of the brain may be first, second and third-order neurons response to the movement of smooth muscle in gallbladder and blood vessels.These PRV labeled neurons may be central autonomic center related to the integration and modulation of reflex control linked to the sensory system monitoring the internal environment, including both visceral sensation and various chemical and physical qualities of the bloodstream. The present morphological results provide that gallbladder meridian and acupoint may be related to the central autonomic pathways.

• 동의생리학회지
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• 제14권2호통권20호
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• pp.199-208
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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) 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 and MTT assay 2. GO, a oxygen radical, increased lipid peroxidation and the amount of LDH. 3. CBY have efficacy of decreasing lipid peroxidation. 4. CBY have efficacy of decreasing the amount of LOH. From the above results, It is concluded that Chilbokyeum has marked efficacy as a treatment for the damages caused in the GO-mediated oxidative process. And Chilbokyeum is thought to have certain pharmacological effects on controlling over aging and treating Dementia. Further clinical study of this pharmacological effects of Chilbokyeum should be complemented.

• 동의생리학회지
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• 제14권2호통권20호
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• pp.117-126
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• 1999

The purpose of this study is to examine the toxic effects caused by Glucose Oxidase(GO) and the effects of herbal extracts such as 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 and MTT assay. 2. GO, a oxygen radical, decreased the amount of neurofilaments and total protein. 3. AR have efficacy of increasing the amount of neurofilament. 4. AR have efficacy of increasing the amount of total protein. From the above results, It is concluded that AR has marked efficacy as a treatment for the damages caused in the GO-mediated oxidative process. And AR is thought to have certain pharmacological effects on controlling over aging. Further clinical study of this pharmacological effects of AR should be complemented.

• 대한물리치료과학회지
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• 제9권3호
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• pp.107-119
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• 2002

Astrocyte, which shares the greatest part of the brain (about 25%), is a land of glial cell that composes the central nervous system along with microglia, ependymal cell and oligodendroglia. It has 7-9nm of fibers in its cytoplasma, which are composed of glial fibrillary acidic protein (GFAP) and vimentin. As for the functions of the astrocyte, it has, so far, been supposed that the astrocyte will play a cytoskeletal role in maintaining the structure of the cerebrum, play a role as a blood-brain barrier so that it can induce migration of the neuron in its development and substances in the blood cannot go into the nervous tissue, and a role of immunology and phagocytosis. However, it was revealed today that it will be a role in preventing expansion of injury by attaching itself to the connective tissue such as the vessel and the pia mater when the nervous tissue or the arachnoid is injured. Microcurrent stimulation can control current, on the basis of A unit. That is, with such devices using it, it is possible to sense, from the outside, the injured current(wound current) of the lesion and to change it into the normal current, thereby promoting the restoration of the cells. In order to examine the effects of microcurrent stimulation on the injured astrocytes in the rabbits, this study was conducted with 24 New Zealand White Rabbit as its subjects, which were divided into 8 animals of the experiment group and 16 animals of the control group. After the animals in the experiment group were fixed to the stereotaxic apparatus, their hair was removed and their premotor area(association area) perforated by the micro-drill for skull-perforation with the depth of 8mm from the scalp. In one week after the injury, 4 animals in the control group and 8 animals in the experiment group were sacrificed and examined with immunohistochemical method. And in three weeks, the remaining 4 animals in the control group and 8 animals in the experiment group were also sacrificed and examined with the same way. The conclusion has been drawn as follows : In the control group sacrificed in one week after the injury, the astrocytes somewhat increased, compared with the normal animals, and in the group sacrificed in three weeks after the injury, they increased more (p < 0.05). The experiment group A in one week showed a little increase, but there was no significant differences, but the experiment group in three weeks showed more increase, compared with the experiment group in one week (p < 0.05). The experiment group B in one week showed more increase than the control group or the experiment group A, and the experiment group in three weeks showed more increase than the experiment group in one week (p < 0.05). Among the astrocytes, fibrous astrocytes were mostly observed, increasing as they are close to the lesion, and decreasing as they are remote from it. The findings show that microcurrent can cause the astrocytes to proliferate and that it will be more effective to stimulate the cervical part somewhat remote from the lesion rather than to directly stimulate the part of the lesion. Thus, microcurrent stimulation can be one of the methods that can activate the reaction of astrocytes, which is one of the mechanism for treating cerebral injury with hemorrhage. Therefore, this study will be used as basic research data for promoting restoration of functions in the patient with injury in the central nervous system.

• Journal of Chest Surgery
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• 제41권4호
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• pp.405-416
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• 2008

배경: 흉부 및 흉복부 대동맥의 수술 중 대동맥 차단은 허혈성 척수 손상에 의한 하반신 마비와 같은 심각한 합병증을 유발할 수도 있어 수술 중 허혈성 척수손상을 예방하기 위한 여러 방법의 연구가 계속 되고 있다. 최근에 허혈성 대뇌 손상 모델에서 신경조직의 막전위 의존성 나트륨채널 길항제가 대뇌 보호 효과가 있다는 보고가 있다. 본 연구는 토끼의 허혈성 척수손상 모델에서 나트륨채널 길항제인 페니토인과 저체온의 척수보호효과를 비교해 보고자 시행되었다. 대상 및 방법: 뉴질랜드산 토끼의 신동맥직하부에서 복부대동맥을 25분간 차단하는 방식으로 척수허혈을 유도하였으며 각 군당 8마리씩 네 군으로 나누었다. 대조군과(S39) 저체온군은(S37) 대동맥 차단시간 동안 직장온도를 각기 $39^{\circ}C$와 $37^{\circ}C$로 일정하게 유지하면서 $22^{\circ}C$ 생리적 식염수만 2 mL/min의 속도로 연속 주입하였으며, 정상체온 및 저체온 페니토인 군은(P39, P37) 앞의 두 군과 동일한 방법으로 하되 생리적 식염수에 페니토인을 녹여 주입하였다(100 mg/50 mL). 수술 후 24시간 및 72시간이 경과한 다음 Tarlov scoring을 통해 신경학적 평가를 시행하였고 마지막 평가 후에는 객관적으로 신경손상의 정도를 정량화하기 위해 척수를 고정 처리하였다. 결과: 페니토인의 역행성 주입에 따른 심각한 문제는 없었으며 대조군에(S39) 속한 모든 동물은 완전 또는 심한 하반신 마비 소견을 보였다. 페니토인과(P39) 저체온(S37)군 모두 대조군에 비해 신경학적 평가는 유사한 정도로 우수한 결과를 보였다(p<0.05). 조직 병리학적 검사 결과, 대조군에 속한 모든 동물은 척수 회백질에서 심한 신경조직 괴사 때 보이는 전형적인 특징을 보여주었으며, TUNEL 염색에 양성인 신경세포도 높은 빈도로 관찰되었으나, 저체온 또는 페니토인 투여 군에서는 괴사현상이 유의한 정도로 감소하였으며, 상대적으로 매우 낮은 빈도의 TUNL 염색 양성세포가 관찰되었다(p<0.05). 그러나 저체온과 페니토인을 병용했을 때의 부가적인 척수보호효과를 조사해 본 결과 신경학적 평가와 조직병리학적 결과 모두 유의한 수준의 부가적인 효과는 없었다. 걸론: 결론적으로, 토끼의 허혈성 척수 손상 모델을 이용하여 페니토인과 저체온의 신경보호효과를 알아본 결과 신경학적 평가와 조직병리학적 검사 결과 모두 부가적인 효과는 보여주지 못했지만 각각의 경우 유사한 정도의 신경보호효과를 보여주었다.