• 대한한의학회지
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• 제26권2호
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• pp.217-230
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• 2005

Objectives: Chungpaesagan-tang (CPSGT), which is frequently used for treating patients of cerebrovascular disease, has not been reported by clinical doctors concerning the effect of neuronal aptosis caused by brain ischemia. To study the effect of CPSGT on focal cerebral ischemia in normal and diabetic rats and SHR, focal cerebral ischemia was induced by transient MCAO, and after onset CPSGT was administrated. Methods: Rats (Sprague-Dawley) were divided into four groups: sham-operated group, MCA-occluded group, CPSGT­administrated group after MCA occlusion, and normal group. The MCA was occluded by intraluminal method. CPSGT was administrated orally twice (l and 4 hours) after middle cerebral artery occlusion. All groups were sacrificed at 24 hours after the surgery. The brain tissue Was stained with $2\%$ triphenyl tetrazolium chloride (TTC) or $1\%$ cresyl violet solution, to examine effect of CPSGT on ischemic brain tissue. The blood samples were obtained from the heart.~. Tumor necrosis $factor-\alpha$ level and interleukin-6 level of serum was measured from sera using enzyme-linked immunoabsorbent assay (ELISA). Then changes of immunohistochemical expression of $TNF-\alpha$ in ischemic damaged areas were observed. Results: In NC+MCAO+CP and DM+MCAO+CP, CPSGT significantly (p<0.01) decreased the number of neuron cells compared to the control group. CPSGT markedly reduced (p<0.01) the infarct size of the forebrain in distance from the interaural line on cerebral ischemia in diabetic rats. CPSGT significantly reduced the $TNF-\alpha$ expression in penumbra region of damaged hemisphere in diabetic rats. Conclusions: CPSGT had a protective effect on cerebral ischemia in SD rats, especially in diabetic rats compared with normal SD rats.

• 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.

• 산업융합연구
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• 제17권4호
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• pp.39-43
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• 2019

마우스 배아 줄기 세포는 신경 세포 분화가 가능한 세포의 대안적인 공급원이 될 수 있으며 잠재적으로 신경계 질환의 치료에 유용하게 사용될 수있다. 우리는 배아 줄기 세포 (ESCs)가 신경 분화를 유도하도록 유도 될 수 있는지를 조사했다. 신경 세포 유도 후, mESC의 표현형이 뉴런의 형태학으로 변하였고, mESCs는 실험쥐 뇌의 측 뇌실로 주입되었다. 이식 된 세포는 뇌의 여러 부위로 이동하였고 중대뇌동맥 결찰에 의한 허혈성 뇌혈관 손상부위에 이식된 줄기세포군이 손상된 피질부위로 집중적으로 이동하여 손상복구 기전을 증가시켰다. mESCs의 뇌내 이식은 MCAO 쥐의 기능적 결손의 감각 및 운동 회복을 유의 적으로 향상시킨다. 이러한 데이터는 이식 된 mESC가 허혈성 미세 환경에서 생존, 이동 및 분화하고 쥐에서 뇌졸중 후 신경 기능 회복을 향상 시킨다는 것을 나타낸다. 따라서 우리는 mESC의 이식이 인간 신경계 손상 및 퇴행성 장애에 대한 강력한 이식 치료법을 제공 할 것으로 기대한다.

• BMB Reports
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• 제49권2호
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• pp.71-72
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• 2016

Focal cortical dysplasia type II (FCDII) is a focal malformation of the developing cerebral cortex and the major cause of intractable epilepsy. However, since the molecular genetic etiology of FCD has remained enigmatic, the effective therapeutic target for this condition has remained poorly understood. Our recent study on FCD utilizing various deep sequencing platforms identified somatic mutations in MTOR (existing as low as 1% allelic frequency) only in the affected brain tissues. We observed that these mutations induced hyperactivation of the mTOR kinase. In addition, focal cortical expression of mutant MTOR using in utero electroporation in mice, recapitulated the neuropathological features of FCDII, such as migration defect, cytomegalic neuron and spontaneous seizures. Furthermore, seizures and dysmorphic neurons were rescued by the administration of mTOR inhibitor, rapamycin. This study provides the first evidence that brain somatic activating mutations in MTOR cause FCD, and suggests the potential drug target for intractable epilepsy in FCD patients.

• 대한한의학회지
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• 제21권3호
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• pp.88-98
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• 2000

Objectives : This study was carried out to evaluate the effect of Boyanghwano-tang Extracts on Reversible Forebrain Ischemia in Mongolian Gerbils. Methods : The water content of cerebral edema and the morphologicalㆍneurocytochemistrical change of neuron in MG were implemented to conduct this study. Results : The change rate of water content by ischemia in the normal group was 78.90% on the third day and 79.12% on the seventh day after an attack of ischemia. The rate in the control group was 80.34% and 81.72%. In the sample group the rate was 79.85% and 80.97%. This is a significant result. According to the result of the optical microscopic examination, the cells seen to be continuous and systematic in the pyramidal cells of hippocampus were changed into discontinuous and unsystematic forms in the control group. But compared with the control group, the cells were less damaged in the sample group. Conclusions : The data shows that the effect of Boyanghwano-tang Extracts on Reversible Forebrain Ischemia in MG is a significant result.

• 한국수정란이식학회:학술대회논문집
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• 한국수정란이식학회 2004년도 제4회 발생공학 국제심포지움 및 학술대회
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• pp.57-58
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• 2004

• Annals of Clinical Neurophysiology
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• 제15권2호
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• pp.59-62
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• 2013

Man-in-the-barrel syndrome (MIBS) is a clinical syndrome of bilateral upper limb weakness with normal lower extremity function. It can be caused by various neurological conditions such as bilateral cerebral hypoperfusion, syringomyelia, motor neuron disease, or cervical myelopathies. We report a patient with MIBS after cervical spinal cord ischemia. It is postulated to be caused by ischemic insults of anterior spinal artery from repeated and prolonged neck extension.

• BMB Reports
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• 제56권2호
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• pp.90-95
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• 2023

Mitochondria are important organelles that regulate adenosine triphosphate production, intracellular calcium buffering, cell survival, and apoptosis. They play therapeutic roles in injured cells via transcellular transfer through extracellular vesicles, gap junctions, and tunneling nanotubes. Astrocytes can secrete numerous factors known to promote neuronal survival, synaptic formation, and plasticity. Recent studies have demonstrated that astrocytes can transfer mitochondria to damaged neurons to enhance their viability and recovery. In this study, we observed that treatment with mitochondria isolated from rat primary astrocytes enhanced cell viability and ameliorated hydrogen peroxide-damaged neurons. Interestingly, isolated astrocytic mitochondria increased the number of cells under damaged neuronal conditions, but not under normal conditions, although the mitochondrial transfer efficiency did not differ between the two conditions. This effect was also observed after transplanting astrocytic mitochondria in a rat middle cerebral artery occlusion model. These findings suggest that mitochondria transfer therapy can be used to treat acute ischemic stroke and other diseases.

• 대한수의학회지
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• 제42권2호
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• pp.137-146
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• 2002

중추신경계는 신경원(neuron)과 이를 지지해주는 신경아교세포(neuroglia)로 이루어져 있다. 발생과정중 신경원의 발달은 NGF(neruv growht factor)에 의해 관찰이 가능하고, 아교세포들중 별모양아교세포는 GFAP(Glial fibrillary acidic protein)항체로 밝혀낼 수 있다. CNTF(Cillary neurotrophic factor)는 이전에는 운동신경원의 발생 및 유지에 있어 중요한 역할을 하는 인자로 알려져 왔으며, 최근에는 발생과정 중 NGF와 GFAP의 역할에 도움을 주는 것으로 알려졌다. 본 연구에서는 이러한 NGF, GFAP, CNTF를 발생과정 중(임신 15,17,19,21일, 출생 1,2,3,일, 1,2,3주)의 몽골리안 저빌의 전뇌에서 시간에 따른 분포를 광학현미경, 형광염색을 통한 공초점현미경 및 전자현미경을 통해 알아보고자 하였다. 전뇌에서 NGF는 발생 19일령에서부터 대뇌피질에서 관찰되기 시작해서 후각망울, 해마체 및 diagonal band에 관찰되었고, 출생 3일령에서 가장 강한 염색성을 보였으며 그 반응은 출생 3주까지도 관찰되었다. GFAP는 출생17일령에서 뇌실로부터 아교세포가 관찰되는 형태가 보였으며, 외측뇌실과 제3뇌실에서부터 피질로 이동하는 형태로 관찰되었다. 또한 후각망울의 과립층, 대뇌피질 및 해마체에서 관찰되었으며, 출생 2일령에서 가장 강한 반응을 나타내었다. CNTF는 신경원과 신경아교세포에서 관찰되었으며, NGF와 GFAP와는 달리 출생 전에서는 관찰되지 않다가 출생 1일령부터 후각망울 및 대뇌피질에서 약하게 관찰되기 시작되었으며, 이러한 반응은 출생 2주령에서 잘 관찰되었다. 전자현미경상에서는 신경원과 신경아교세포에서 특징적인 구조는 관찰되지 않았으나, 각각의 항체에 대한 반응이 나타난 세포에서는 사립체와 형질내세망과 같은 세포소기관들이 많이 관찰되었다. 이러한 Mongolian gerbil 전뇌에서의 NGF, GFAP 및 CNTF의 분포는 비슷한 임신일령의 설치류와 거의 유사하게 관찰되었으며, 배아과정 및 출생 후 발달에 따른 전뇌에서의 신경원과 신경아교세포에서의 분포를 볼 수 있었다.

• 동의신경정신과학회지
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• 제21권1호
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• pp.109-124
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• 2010

Objectives: This experiment was designed to investigate the effect of the InSamYangYoung-tang(Renshenyangrongtang) extract on $A{\beta}$-induced AD model. Methods: The effects of the InSamYangYoung-tang(Renshenyangrongtang) extract on neural damages of cultured PC12 cells induced by $A{\beta}$ were investigated. The effects of the InSamYangYoung-tang(Renshenyangrongtang) extract on neural damages of hippocampal and cortical neurons in the mouse induced by $\beta$-amyloid were investigated. Results: 1. $A{\beta}$ treatment into neuronal cells activated cell death pathway when analyzed by MTT assay and by histological analysis. Then InSamYangYoung-tang(Renshenyangrongtang) treatment improved cell survival to a similar level as in normal group. 2. $A{\beta}$ treatment increased caspase 3 protein levels but decreased phospho-Erk1/2 in neuronal cells. InSamYangYoung-tang(Renshenyangrongtang) treatment reversed the production levels of two proteins close to those in normal group. 3. $A{\beta}$ treatment induced the atrophy of neuronal cells in terms of neuronal processes and cell body shrinkage, but InSamYangYoung-tang(Renshenyangrongtang) greatly improved their morphology. 4. Neuroprotective activity, as observed in InSamYangYoung-tang(Renshenyangrongtang)-treated groups, was similarly observed in cells treated with galantamine which was used as a positive control. Moreover, overall recovery pattern by InSamYangYoung-tang(Renshenyangrongtang) was similar between cultured PC12 cells and in vivo hippocampal and cerebral cortical neurons in the mouse brain. Conclusions: This experiment shows that the InSamYangYoung-tang(Renshenyangrongtang) may play a protective role in neural tissues damaged by cytotoxic substances. Since neuronal damage seen in degenerative brains such as AD are largely unknown, the current data may provide possible insight into therapeutic strategies for AD treatments. InSamYangYoung-tang(Renshenyangrongtang) might be effective for the treatment of AD. Investigation into the clinical use of the InSamYangYoung-tang(Renshenyangrongtang) for AD is suggested for future research.