• The Korean Journal of Physiology and Pharmacology
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• v.10 no.4
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• pp.173-180
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• 2006

Microglial activation is thought to play a role in the pathogenesis of many brain disorders. Therefore, understanding the response of microglia to noxious stimuli may provide insights into their role in disorders such as stroke and neurodegeneration. Many genes involved in this response have been identified individually, but not systematically. In this regards, the microarray system permitted to screen a large number of genes in biological or pathological processes. Therefore, we used microarray technology to evaluate the effect of oxygen glucose deprivation (OGD) and reperfusion on gene expression in microglia under ischemia-like and activating conditions. Primary microglial cultures were prepared from postnatal mice brain. The cells were exposed to 4 hrs of OGD and 1 h of reperfusion at $37^{\circ}C$. Isolated mRNA were run on GeneChips. After OGD and reperfusion, ＞2-fold increases of 90 genes and ＞2-fold decrease of 41 genes were found. Among the genes differentially increased by OGD and reperfusion in microglia were inflammatory and immune related genes such as prostaglandin E synthase, $IL-1{\beta}$, and $TNF-{\alpha}$. Microarray analysis of gene expression may be useful for elucidating novel molecular mediators of microglial reaction to reperfusion injury and provide insights into the molecular basis of brain disorders.

• Journal of Korean Neurosurgical Society
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• v.50 no.3
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• pp.252-255
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• 2011

Authors report a case of a painless acute dissecting aneurysm of the descending aorta in a patient who presented with unexplained hypotension followed by simultaneous paraplegia and right arm monoparesis. To our knowledge, case like this has not been reported previously. Magnetic resonance imaging of the brain and spine revealed hemodynamic cerebral infarction and extensive cord ischemia, respectively. Computerized tomography angiography confirmed a dissecting aneurysm of the descending aorta. The cause of the brain infarction may not have been embolic, but hemodynamic one. Dissection-induced hypotension may have elicited cerebral perfusion insufficiency. The cause of cord ischemia may be embolic or hemodynamic. The dissected aorta was successfully replaced into an artificial patch graft. The arm monoparesis was improved, but the paraplegia was not improved. In rare cases of brain and/or spinal cord infarction caused by painless acute dissecting aneurysm of the aorta, accurate diagnosis is critical because careless thrombolytic therapy can result in life-threatening bleeding.

• The Journal of Korean Medicine
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• v.27 no.2 s.66
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• pp.70-85
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• 2006

Objectives; This study examined the neuroprotective effect of Hyulbuchookautang (血府逐瘀湯, HBCAT)against neural damage following focal cerebral infarction. Methods : Sprague-Dawley Rats were induced with focal cerebral infarction by temporal middle cerebral artery occlusion (MCAO). The rats were divided into 2 groups. We treated extract of HBCAT to one group after operation (sample group), and the other group wasn't treated after operation (control group). We observed neurological scores and TIC-stained infarct area, total infarct volume in brain sections and Bax-positive neurons, HSP70- positive neurons in brain regions. Results : HBCAT treatment at 3 days after MCAO reduced neurological scores induced by MCAO. HBCAT treatment at 5 days after MCAO reduced TTC-stained infarct area in brain sections induced by MCAO. HBCAT treatment at 5 days after MCAO reduced total infarct volume in brain sections induced by MCAO. HBCAT treatment after MCAO reduced Bax-positive neurons in cortex infarct core and cortex infarct penumbra and caudo-putamen of brain regions induced by MCAO. HBCAT treatment after MCAO reduced HSP70- positive neurons in cortex infarct penumbra of brain regions induced by MCAO. Conclusions : These results suggest that HBCAT has a neuroprotective effect against focal cerebral ischemia.

• Korean Journal of Pharmacognosy
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• v.31 no.4
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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.

• The Korean Journal of Physiology and Pharmacology
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• v.5 no.3
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• pp.205-212
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• 2001

It has been proposed that nitirc oxide is involved in the pathogenesis of cerebral ischemia-reperfusion. Because superoxide production is also enhanced during reperfusion, the cytotoxic oxidant peroxynitrite could be formed, but it is not known if this occurs following global forebrain ischemia-reperfusion. We examined whether peroxynitrite generation is increased in the vulnerable regions after forebrain ischemia-reperfusion. Transient forebrain ischemia was produced in the conscious rat by four-vessel occlusion. Rats were subjected to 10 or 15 min of forebrain ischemia. Immunohistochemical method was used to detect 3-nitrotyrosine, a marker of peroxynitrite production. 3-Nitrotyrosine immunoreactivity was enhanced in the hippocampal CA1 area 3 days after reperfusion. Furthermore, in rats subjected to ischemia for 15 min, this change was also observed in the lateral striatal region and the lateral septal nucleus $2{\sim}3$ days after reperfusion. The cresyl violet staining of adjacent sections showed that neuronal cell death was induced in parallel with the nitrotyrosine immunoreactivity in the hippocampal CA1 area and the lateral striatal region. Our findings suggest that oxygen free radical accumulation and consequent peroxynitrite production play a role in neuronal death caused by cerebral ischemia-reperfusion.

• 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.

• Proceedings of the Ginseng society Conference
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• 1998.06a
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• pp.21-30
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• 1998

Ginseng root has been considered to prevent neuronal degeneration associated with brain ischemia, but experimental proof in support of this speculation is limited. Moreover, few studies have compared the neuroprotective actions of ginseng ingredients with those of peptide growth factors and cytokines isf vivo. Using a gerbil forebrain ischemia model, we demonstrated that the oral administration of red ginseng powder before an ischemic insult prevents delayed neuronal death in the hippocampal CAI field and that a neuroprotective molecule within red ginseng powder is ginsenoside Rbl. The neurotrophic effect of ginsenoside Rbl, when examined in the gerbil ischemia model and in neuronal cultures was as potent as or more potent than the effects of epidermal growth factor, ciliary neurotrophic factor, erythropoietin, prosaposin, interleukin-6 and interleukin-3. Besides the protection of hippocampal CAI neurons against brain ischemia/repercussion injuries, ginsenoside Rbl was shown to prevent place navigation disability, cortical infarction and secondary thalamic degeneration in stroke-prone spontaneous hypertensive rats with permanent occlusion of the unilateral middle cerebral artery distal to the striate branches. These findings may validate the empirical use of ginseng root for the treatment of cerebrovascular diseases

• The Korea Journal of Herbology
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• v.23 no.3
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• pp.1-9
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• 2008

Objectives : This research was performed to investigate protective effect of Sophora Subprostrata against transient global ischemic damage after 5-min two vessel occlusion. Methods : Gerbils were divided into three groups: Normal group, 5-min two vessel occlusion (2VO) group, Sophora Subprostrata administrated group after 2VO. The CCAs were occluded by microclip for 5min. Sophora Subprostrata was administrated orally(12mg/ml) for 7 days after 2VO. The histological and immunohistochemistrical analysis was performed at 72 hours and 7 days after the surgery each. For histological analysis, the brain tissue was stained with 1% cresyl violet solution and Immunohistochemistry for BAX and Bcl-2 was carried out to examine effect of Sophora Subprostrata on ischemic brain tissue. Results : The results showed that (1) Sophora Subprostrata has the protective effect against ischemia in CA1 area of the gerbil hippocampus 7 days after 5-minute occlusion, (2) the treatment of Sophora Subprostrata inhibits the expression of Bax relatively after 2VO-induced ischemia. That protective effect of the Sophora Subprostrata seems to be performed by regulating the proportion of Bax and Bcl-2 protein, (3) in hypoxia/reperfusion model using PC12 cell, the Sophora Subprostrata extract has the protective effect against ischemia in the dose of $2{\mu}/m{\ell}$ and $20{\mu}/m{\ell}$.This study suggests that Sophora Subprostrata has neuroprotective effect against neuronal damage following cerebral ischemia in vivo with a widely used experimental model of cerebral ischemia in Mongolian gerbils and that Sophora Subprostrata regulates the proportion of Bax and Bcl-2 protein following ischemia. And, Sophora Subprostrata extract has protective effects also on a hypoxia/reperfusion cell culture model using PC12 cell. Conclusions : Sophora Subprostrata has protective effects against ischemic brain damage at the early stage of ischemia.

• Journal of Korean Neurosurgical Society
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• v.39 no.4
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• pp.300-302
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• 2006

"Stunning" represents prolonged contractile depression of any muscular component after alleviation of severe ischemia, as shown in reperfusion following acute myocardial ischemia or ischemic stroke. Clinically, it presents with no or delayed recovery past to thrombolytic therapy but its pathogenic mechanism is not fully uncovered yet. We describe a unique case of a 63-year-old woman, who was undertaken endovascular coiling for the aneurysms, deteriorated several hours later without known cause, and showed delayed clinical improvement over the next 3 days following thrombolysis. Immediate post-thrombolysis magnetic resonance imaging scan showed no apparent abnormality except for high signal intensity within the corresponding hemisphere. Reversible but delayed nature of " brain stunning" can be explained by these images and it seems to be caused by a certain type of reperfusion injury.

• Journal of Veterinary Clinics
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• v.26 no.1
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• pp.104-108
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• 2009

Global cerebral ischemia occurs commonly in patients who have a variety of clinical conditions including cardiac arrest and shock. Cerebral ischemia results in a rapid depletion of energy stores that triggers resulting in excitotoxic death. Imaging studies of the brain with computed tomography(CT) or magnetic resonance imaging(MRI) are necessary to confirm the clinical neurolocalization, identify any associated mass effect, and rule out other causes of focal brain disorders. Cardiopulmonary arrest was occurred by propofol anesthesia in a 1 year old, intact female Beagle dog. After successful cardiopulmonary resuscitation was performed within 5 minutes, clinical signs such as vocalization, paddling, opisthotonus and seizure were represented. At the 12th day, CT and MRI examinations of the brain were performed to evaluate the brain. After euthanasia, histopathologic examination was performed. On transverse image of CT, lesions appeared as a hypodense in the right dorsal surface of the frontal lobe and level of optic canal, and dorsomedial surface of occipital lobe of cerebrum. No contrast enhancement was represented following intravenous contrast administration. On MR images of brain, the lesions were seen as a hyperintense on T2-weighted(T2W) images and a isointense or mild hypointense on T1-weighted(T1W) images. Hyperintense lesions both T2W and T1W images were observed at the surrounding cerebral sulcus. There was no significant signal changes on contrast T1WI. Histopathologic examination after euthanasia revealed that the lesion was necrosis of the cerebral cortex caused by cerebral ischemia.