• Biomolecules & Therapeutics
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• v.5 no.3
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• pp.306-315
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• 1997

In order to investigate pharmacological properties of ι -muscone, effects of ι-muscone and musk on cerebral ischemia and central nervous system were compared. Cerebral ischemia insult was performed using unilateral carotid artery occlusion in Mongolian gerbils. The histological observations showed a preventive effect of the ι-muscone treatment with ischemia-induced brain damage. The ATP in brain tissue was decreased in vehicle-treated ischemic gerbils. This decrease was prevented by the ι-muscone treatment. In contrast to what was seen with ATP, the lactate and lipid peroxide were both elevated in vehicle-treated ischemic gerbils.˙ This elevation was prevented by the ι-muscone treatment. While ι-muscone had no effects on the hexobarbital-induced sleeping time and the convulsions induced by electric shock, pentetrazol and strychnine, it had effect on rotarod test and spontaneous activity test. Respiration rate and depth were increased by the ι-muscone treatment. Furthermore, ι-muscone showed anti-stress effect. Our findings suggest that the pharmacological profile of ι-muscone on cerebral ischemia and central nervous system are similar to that of musk.

• The Journal of Korean Medicine
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• v.28 no.2 s.70
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• pp.44-53
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• 2007

Objectives : This study examined the neuroprotective effect of Hyulbuchookau-tang (血府逐瘀湯, HBCAT) against neural damage following global cerebral infarction. Methods : Sprague-Dawley rats were induced with global cerebral infarction by occlusion of the bilateral common carotid artery with hypotension (CCAO). The rats were divided into 3 groups. We treated extract of HBCAT to one group after operation (sample group), one group wasn't induced with ischemic damage after operation (sham group), and one group was induced with ischemic damage after operation (control group) but not treated. We observed neurological scores and cresyl violet-stained hippocampus CAl area, TUNEL-positive neurons, and Bax-positive neurons in brain regions. Results : HBCAT treatment after CCAO increased pyramidal neurons in CAl hippocampus induced by CCAO. HBCAT treatment after CCAO reduced Bax-positive neurons in CAl hippocampus of brain regions induced by CCAO. HBCAT treatment after CCAO wasn't effective for HSP70-positive neurons in CAl hippocampus induced by CCAO. Conclusions : These results suggest that HBCAT has a neuroprotective effect against global cerebral ischemia.

• Biomolecules & Therapeutics
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• v.5 no.4
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• pp.402-411
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• 1997

ln order to investigate pharmacological properties of New Woohwangchungsimwon Liquid (NCL) and Woohwangchungsimwon Liquid (CL), effects of NCL and CL on cerebral ischemia and central nervous system were compared. Cerebral ischemia insult was performed using unilateral carotid artery occlusion in Mongolian gerbils. The histological observations showed a preventive effect of NCL and CL treatments with ischemia-induced brain damage. The ATP in brain tissue was decreased in vehicle-treated ischemic gerbils. This decrease was prevented by CL treatment. In contrast to what was seen with ATP, the lactate and lipid peroxide were both elevated in vehicle-treated ischemic gerbils. This elevation was inhibited by NCL and CL treatments. While NCL and CL had no effects on the hexobarbital-induced sleeping time, they prevented the seizures induced by electric shock and pentetrazol. NCL and CL showed sedative effect in rotarod and spontaneous activity test. Respiration rate and depth were increased at the high dose of NCL and CL. Furthermore, NCL and CL showed anti-stress effect. Our findings suggest that the pharmacological profile of NCL on cerebral ischemia and central nervous system are similar to that of CL.

• Archives of Reconstructive Microsurgery
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• v.8 no.2
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• pp.170-175
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• 1999

Objective : Extracranial-intracranial(EC-IC) microvascular anastomosis was performed in 18 patients with hemodynamic cerebral ischemia and traumatic cerebral aneurysm, the aim of this retrospective study was to assess its value in neurosurgical field. Method : Of 18 cases, 17 case were hemodynamic cerebral ischemia and one was traumatic cerebral aneurysm. There were 14 superficial temporal artery(STA)-to-middle cerebral artery(MCA) anastomosis, 3 saphenous vein graft bypass(2 external carotid artery(ECA)-to-MCA, 1main trunk of the STA-to-MCA) and 1 radial artery bypass(ECA-to-MCA). Results : Bypass patency was confirmed by postoperative angiography in all cases except for two cases, postoperative cerebral blood flow of ischemic brain showed significant increased in all cases with good patency through bypass. Conclusion : Revascularization by EC-IC microvascular anastomosis to the ischemic brain eliminated ischemia and was associated with excellent good outcome and good patency rates.

• Biomolecules & Therapeutics
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• v.7 no.1
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• pp.79-88
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• 1999

In order to investigate pharmacological properties of New Wonbang Woohwangchungsimwon Liquid(NSCL) and Wonbang Woohwangchungsimwon Liquid(SCL), the effects of NSCL and SCL on cerebral ischemia and central nervous system were compared. Cerebral ischemia insult was performed using unilateral carotid artery occlusion in mongolian gerbils. The histological observations showed a preventive effect of NSCL and SCL treatments with ischemia-induced brain damage. The ATP in brain tissue was decreased in vehicle-treated ischemic gerbils. This decrease was prevented by NSCL and SCL treatment. In contrast to what was seen with ATP, lipid peroxide were elevated in vehicle-treated ischemic gerbils. This elevation was inhibited by NSCL and SCL treatments. While NSCL and SCL had no effects on the hexobarbital-induced sleeping time, they showed sedative effect in rotarod and spontaneous activity test. NSCL and SCL prevented the seizures induced by electric shock and strychnine, but the effect of NSCL was less than that of SCL. Furthermore, NSCL and SCL showed anti-stress effect. Our findings suggest that the pharmacological profiles of NSCL on cerebral ischemia and central nervous system are similar to those of SCL.

• Biomolecules & Therapeutics
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• v.28 no.2
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• pp.152-162
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• 2020

Cerebral ischemia exhibits a multiplicity of pathophysiological mechanisms. During ischemic stroke, the reactive oxygen species (ROS) concentration rises to a peak during reperfusion, possibly underlying neuronal death. Recombinant human erythropoietin (EPO) supplementation is one method of treating neurodegenerative disease by reducing the generation of ROS. We investigated the therapeutic effect of PEGylated EPO (P-EPO) on ischemic stroke. Mice were administered P-EPO (5,000 U/kg) via intravenous injection, and middle cerebral artery occlusion (MCAO) followed by reperfusion was performed to induce in vivo ischemic stroke. P-EPO ameliorated MCAO-induced neurological deficit and reduced behavioral disorder and the infarct area. Moreover, lipid peroxidation, expression of inflammatory proteins (cyclooxygenase-2 and inducible nitric oxide synthase), and cytokine levels in blood were reduced by the P-EPO treatment. In addition, higher activation of nuclear factor kappa B (NF-κB) was found in the brain after MCAO, but NF-κB activation was reduced in the P-EPO-injected group. Treatment with the NF-κB inhibitor PS-1145 (5 mg/kg) abolished the P-EPO-induced reduction of infarct volume, neuronal death, neuroinflammation, and oxidative stress. Moreover, P-EPO was more effective than EPO (5,000 U/kg) and similar to a tissue plasminogen activator (10 mg/kg). An in vitro study revealed that P-EPO (25, 50, and 100 U/mL) treatment protected against rotenone (100 nM)-induced neuronal loss, neuroinflammation, oxidative stress, and NF-κB activity. These results indicate that the administration of P-EPO exerted neuroprotective effects on cerebral ischemia damage through anti-oxidant and anti-inflammatory properties by inhibiting NF-κB activation.

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.3
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• pp.279-286
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• 1998

It has been well documented that transient forebrain global ischemia causes selective neuronal degeneration in hippocampal CA1 pyramidal neurons with a delay of a few days. The mechanism of this delayed hippocampal CA1 pyramidal neuronal death (DND) is still controversial. To delineate the mechanisms of the DND, the effects of treatment with MK-801, an NMDA receptor antagonist, kynurenic acid, a NMDA/non-NMDA receptor antagonist, and/or cycloheximide, a protein synthesis inhibitor, on the DND were investigated in male Wistar rats. To examine the participation of apoptotic neuronal death in the DND, TUNEL staining was performed in ischemic brain section. Global ischemia was induced by 4-vessel occlusion for 20 min. All animals in this study showed the DND 3 and 7 days after the ischemic insult. The DND that occured 3 days and 7 days after the ischemia were not affected by pretreatment with MK-801 (1 mg/kg), but markedly attenuated by the pretreatment with kynurenic acid (500 mg/kg). Treatment with cycloheximide (1 mg/kg) also markedly inhibited the DND. The magnitudes of attenuation by the two drugs were similar. The magnitude of attenuation by co-treatments with kynurenic acid and cycloheximide was not greater than that with any single treatment. TUNEL staining was negative in the sections obtained 1 or 2 days after the ischemic insults, but it was positive at hippocampal CA1 pyramidal cells in sections collected 3 days after the ischemia. These results suggested that the DND should be mediated by the activation of non-NMDA receptor, not by the activation of NMDA receptor and that the activation of AMPA receptor should induce the apoptotic process in the DND.

• Investigative Magnetic Resonance Imaging
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• v.19 no.1
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• pp.31-36
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• 2015

Purpose: To compare the depiction of brain metastases on contrast-enhanced images with 7.0 tesla (T) and at 1.5T MRI. Materials and Methods: Four consecutive patients with brain metastases were scanned on 7.0T whole-body scanner and 1.5T MRI. A 3D T1-weighted gradient echo sequence (3D T1-GRE) at 1.5T (voxel size = $0.9{\times}0.9{\times}1.5mm^3$ after double-dose, gadoterate meglumine, Gd-DOTA) was compared to a 7.0T 3D T1-GRE sequence (voxel size = $0.4{\times}0.4{\times}0.8mm^3$, single-dose Gd-DOTA) in four patients after a 5 minute delay. The number of contrast-enhancing metastases in MPRAGE images was compared in each patient by two radiologists in consensus. We measured contrast ratio of enhancing brain metastases and white matter in 1.5T and 7.0T. Results: In all four patients 7.0T 3D T1-GRE images after single-dose Gd-DOTA and 1.5T after double-dose Gd-DOTA depicted 11 brain metastases equally. In the quantitative analysis of contrast ratios of enhancing brain metastases and white matter, the 1.5T 3D T1-GRE after double-dose showed an increased contrast ratio compared to 7.0T 3D T1-GRE after single-dose ($0.961{\pm}0.571$ versus $0.885{\pm}0.494$; n = 11 metastases). But this difference was not statistically significant (P = 0.711). Conclusion: Our preliminary results indicate that 7.0T single-dose Gd-enhanced images were not different to 1.5T double-dose Gd-enhanced images for the detection of brain metastases.

• Clinical and Experimental Pediatrics
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• v.56 no.7
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• pp.271-274
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• 2013

Brain insults, including neurotrauma, infection, and perinatal injuries such as hypoxic ischemic encephalopathy, generate inflammation in the brain. These inflammatory cascades induce a wide spectrum of cytokines, which can cause neuron degeneration, have neurotoxic effects on brain tissue, and lead to the development of seizures, even if they are subclinical and occur at birth. Cytokines are secreted by the glial cells of the central nervous system and they function as immune system mediators. Cytokines can be proinflammatory or anti-inflammatory. Interleukin (IL)-$1{\beta}$ and IL-8 are proinflammatory cytokines that activate additional cytokine cascades and increase seizure susceptibility and organ damage, whereas IL-1 receptor antagonist and IL-10 act as anti-inflammatory cytokines that have protective and anticonvulsant effects. Therefore, the immune system and its associated inflammatory reactions appear to play an important role in brain damage. Whether cytokine release is relevant for the processes of epileptogenesis and antiepileptogenesis, and whether epileptogenesis could be prevented by immunomodulatory treatment should be addressed in future clinical studies. Furthermore, early detection of brain damage and early intervention are essential for the prevention of disease progression and further neurological complications. Therefore, cytokines might be useful as biomarkers for earlier detection of brain damage in high-risk infants.

• The Journal of Pediatrics of Korean Medicine
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• v.23 no.3
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• pp.241-262
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• 2009

Objectives This study is designed to investigate the effects of Jujadokseo-hwan on the brain ability and inducing oxidative stresses. Methods We measured the changes of regional cerebral blood flow and mean arterial blood pressure. Then we analyzed histological examination, immunohistochemistric response and anti-oxidant activity of Jujadokseo-hwan. Results 1. Treatment of Jujadokseo-hwan significantly increased regional cerebral blood flow but decreased mean arterial blood pressure. 2. Treatment of Jujadokseo-hwan-induced increase of regional cerebral blood flow was significantly inhibited by pretreatment with indomethacin (1 mg/kg, i.p.), an inhibitor of cyclooxygenase. 3. In histological examination through TTC stain, group I was no change, but group II showed that discolored in the most cortical part. Group III showed that decreased discolor in the cortical part. 4. In immunohistochemistric response of BDNF, group II showed that lower response effect. Group III showed that increase response effect. 5. Treatment of Jujadokseo-hwan increased proliferation rates of Glial cell effectively 6. Treatment of Jujadokseo-hwan accelerated proliferation rates of C6 cells in vitro. In addition, protective effects on cell death induced by paraquat, rotenone and hydrogen peroxide. In addition, activity of SOD were increased by treatment with Jujadokseo-hwan. Conclusions In conclusion, Jujadokseo-hwan can improve of the brain ability, learning ability, memory ability and induce ischemic brain injuries.