• Reproductive and Developmental Biology
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• v.35 no.2
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• pp.167-174
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• 2011

Acute ischemic stroke results from sudden decrease or loss of blood supply to an area of the brain, resulting in a coinciding loss of neurological function. The antioxidant action of melatonin is an important mechanism among its known effects to protective activity during ischemic/reperfusion injury. The focus of this research, therapeutic efficacy of melatonin on recovery of neurological function following long term treatment in ischemic brain injured rats. Male Sprague-Dawley rats (n=40; 8 weeks old) were divided into the control group, and MCAo groups (Vehicle, MT7 : MCAo+ melatonin injection at 7:00, MT19 : MCAo+melatonin injection at 19:00, and MT7,19 : MCAo+melatonin injection at 7:00 and 19:00). Rat body weight and neurological function were measured every week for 8 weeks. After 8 weeks, the rats were anesthetized with a mixture of zoletil (40 mg/kg) and xylazine (10 mg/kg) and sacrificed for further analysis. Tissues were then collected for RNA isolation from brain tissue. Also, brain tissues were analyzed by histological procedures. We elucidated that melatonin was not toxic in vital organs. MT7,19 was the most rapidly got back to mild symptom on test of neurological parameter. Also, exogenous melatonin induces both the down-regulation of detrimental genes, such as NOSs and the up-regulation of beneficial gene, including BDNF during long term administration after focal cerebral ischemia. Melatonin treatment reduced the loss of primary motor cortex. Therefore, we suggest that melatonin could be act as prophylactic as well as therapeutic agent for neurorehabilitative intervention.

• The Journal of Internal Korean Medicine
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• v.29 no.3
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• pp.629-640
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• 2008

Objective : The purpose of this study was to investigate the neuroprotective effect of Jukryuk on 4-vessel occlusion(4-VO) and middle cerebral artery (MCA) ischemia. Method : After administration of Jukryuk, we compared the Jukryuk-treated group, the control, and the sham groups, in view of several points as follows 1) We evaluated the damage characterized by coagulative cell change of pyramidal neurons and pronounced gliosis in each group 2) We counted the number of normal pyramidal shapes after ischemia in each group 3) Immunohistochemistry (cyclooxygenase-2) 4) In focal ischemic injury model, we measured the volume of ischemic area Results : In this experiment, the effect of Jukryuk was determined to be protecting neuron cell shape, reducing the number of neuron cells damaged by ischemia and the volume of the ischemic area. In immunohistochemistry, Jukryuk reduced cyclooxygenase-2 expression Conclusions : According to this study, Jukryuk can protect neuron cells from injury by cerebrovascular ischemia.

• Journal of Acupuncture Research
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• v.25 no.1
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• pp.1-14
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• 2008

Objectives : Delayed neuronal death(DND) of pyramidal neuronsin the CA1 regions of the hippocampus has been extensively studied following global brain ischemia, whereas little is known about DND in this highly vulnerable brain region after focal brain ischemia. The aim of the present study was to investigate the effect of Gastrodiae Elata(GA) pharmacopuncture on hippocampal neuronal apoptosis in rats with focal brain ischemic injury. Materials and methods : The neuroprotective effects of water extracts of GA were investigated in middle cerebral artery occlusion(MCAo) of Sprague-Dawley(SD) rats. Seventy-five healthy SD ratswere randomly divided into five groups following MCAo : control group with focal ischemia, saline injection group, pharmacopuncture group GA-1($0.0007mg/m{\ell}/g$), pharmacopuncture group GA-2($0.00035mg/m{\ell}/g$), pharmacopuncture group GA-3($0.00014mg/m{\ell}/g$). Results : The intensity of mGluR5 increased in the GA-1 group. The intensity of Bax and the Bax/Bcl-2 ratio decreased in the GA-1 group. The intensity of Bcl-2 increased in all the GA groups. The density of neurons stained by Cresyl violet and ChAT increased in the GA-1 group. Conclusions : Our study suggests that GA pharmacopuncture at $GB_{20}$ showed anti-apoptotic and neuroprotective effects on cholinergic neuronsin focal cerebral ischemia caused by stroke in SD rats.

• The Korean Journal of Physiology and Pharmacology
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• v.14 no.6
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• pp.435-440
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• 2010

Valproic acid (VPA) is a well-known anti-epileptic and mood stabilizing drug. A growing number of reports demonstrate that VPA is neuroprotective against various insults. Despite intensive efforts to develop new therapeutics for stroke over the past two decades, all treatments have thus far failed to show clinical effect because of treatment-limiting side effects of the drugs. Therefore, a safety-validated drug like VPA would be an attractive candidate if it has neuroprotective effects against ischemic insults. The present study was undertaken to examine whether pre- and post-insult treatments with VPA protect against brain infarct and neurological deficits in mouse transient (tMCAO) and permanent middle cerebral artery occlusion (pMCAO) models. In the tMCAO (2 hr MCAO and 22 hr reperfusion) model, intraperitoneal injection of VPA (300 mg/kg, Lp.) 30 min prior to MCAO significantly reduced the infarct size and the neurological deficit. VPA treatment immediately after reperfusion significantly reduced the infarct size. The administration of VPA at 4 hr after reperfusion failed to reduce the infarct size and the neurological deficit. In the pM CAO model, treatment with VPA (300 mg/kg, i.p.) 30 min prior to MCAO significantly attenuated the infarct size, but did not affect the neurological deficit. Western blot analysis of acetylated H3 and H4 protein levels in extracts from the ischemic cortical area showed that treatment with VPA increased the expression of acetylated H3 and H4 at 2 hrs after MCAO. These results demonstrated that treatment with VPA prior to ischemia attenuated ischemic brain damage in both mice tMCAO and pMCAO models and treatment with VPA immediately after reperfusion reduced the infarct area in the tMCAO model. VPA could therefore be evaluated for clinical use in stroke patients.

• Journal of Korean Neurosurgical Society
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• v.57 no.6
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• pp.401-407
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• 2015

The nonprogressive unilateral intracranial arteriopathy known as transient (focal) cerebral arteriopathy is not a well-recognized arteriopathy among practitioners of Korea and Japan, although it cannot be easily differentiated from early moyamoya disease. This review summarizes the nomenclature, pathophysiology, diagnostic evaluation, clinico-radiological features, and management of nonprogressive (reversible or stable) unilateral arteriopathy based on the relevant literature and our own experiences. Nonprogressive unilateral arteriopathy should be strongly suspected in children presenting with basal ganglia infarction and arterial beading. The early identification of patients likely to have nonprogressive or progressive arteriopathy would ensure proper management and guide further research for secondary stroke prevention.

• Bulletin of the Korean Chemical Society
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• v.33 no.7
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• pp.2443-2446
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• 2012

• The Journal of Korean Medicine
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• v.24 no.2
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• pp.204-212
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• 2003

Current therapy for acute ischemic stroke is highly focused on neuroprotective agents, and many herbal medicines have been challenged for experimental models. The aim of this study is to investigate whether Angelicae gigantis Radix can protect nerve cells against ischemic neural damage of middle cerebral artery occlusion (MCAO) in rats' brains. Rats were treated with Angelicae gigantis Radix immediately after 2 hours of MCAO for 7 days. On the 7th day, the brains of the rats were sliced through the hippocampus and dyedby c-Fos immunohistochemistry stain and cresyl violet stain for microscopic examination. The number of viable neurons and c-Fos immunoreactive cells in CA1 regions was counted. MCAO caused significant decrease in density of neurons and c-Fos immunoreactive cells compared to those of sham-operated rats. Administration of Angelicae gigantis Radix significantly elevated MCAO-induced decrease in density of neurons and c-Fos immunoreactive cells. These results suggest that the neuroprotective effect of Angelicae gigantis Radix against focal cerebral ischemia is related to c-Fos gene expression. Thus, these findings indicate that Angelicae gigantis Radix can be used for treatment and prevention of cerebral ischemia.

• Proceedings of the Korean Society of Applied Pharmacology
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• 2003.11a
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• pp.62-62
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• 2003

It is now convincing that free radical generation is involved in the pathophy siological mechanisms of ischemic stroke, particularly in ischemia-reperfusion injury. The present study, therefore, examined neuroprotective effect of aloesin isolated from Aloe vera, which was known to have antioxidative activity, in a rat model of transient focal cerebral ischemia. Transient focal cerebral ischemia was induced by occlusion of middle cerebral artery for 2 hr with a silicone-coated 4-0 nylon monofilament in male Sprague-Dawley rats under isoflurane anesthesia Aloesin (1, 3, 10, 30 and 50 mg/kg/injection) was administered intravenously 3 times at 0.5, 2 and 4 hr after onset of ischemia. Neurological score was measured 24 hr after onset of ischemia immediately before sacrifice. Seven serial coronal slices of the brain were stained with 2,3,5-triphenyltetrazolium chloride and infarct size was measured using a computerized image analyzer. Treatment with the close of 1 or 50 mg/kg did not significantly reduce infarct volume compared with the saline vehicle-treated control group. However, treatments with the closes of 3 and 10 mg/kg significantly reduced both infarct volume and edema by approximately 47% compared with the control group, producing remarkable behavioral recovery effect. Treatment with the close of 30 mg/kg also significantly reduced infarct volume to a lesser extent by approximately 33% compared with the control group, but produced similar degree of behavioral recovery effect. In addition, general pharmacological studies showed that aloesin was a quite safe compound. The results suggest that aloesin can serve as a lead chemical for the development of neuroprotective agents by providing neuroprotection against focal ischemic neuronal injury.

• Proceedings of the Korean Society of Embryo Transfer Conference
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• 2002.11a
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• pp.111-111
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• 2002

Stroke occurs when local thrombosis, embolic particle or the rupture of blood vessele interrupts the blood floe to the brain. $\beta$-estradiol 17-valerate has been reported to exert neuroprotective effects when administered before an ischemic insult. Recently, the pathophysiology of cerebral ischemia has been studied extensively in rat with various methods. In the present study, we investigates whether $\beta$-estrodiol 17-valerate can protect against brain injury. RNA sample were extracted from the hippocampus of female rat, reverse-transcription in the presence of [$\alpha$32p] dATP. Differential gene express-ion profiles were revealed (Bone morphogenetic protein type 1A receptor, Protein disulphide isomerase, Leukemia inhibitor factor receptor, cytochrome bc- 1 complex-x core P, thiol-specific antioxidant protein). RT-PCR was used to validate the relative expression pattern obtained by the cDNA array. The precise relationship between the early expression of recovery genes and stroke is a matter of luther investigation. This Study was supported by the Korea Science and Engineering Foundation(KOSEF) through the Biohealth Products Research Center(BPRC), Inje University, Korea.

• Physical Therapy Rehabilitation Science
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• v.2 no.2
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• pp.87-91
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• 2013

Objective: The present study was aimed at determining the effect of physical training on glutamate transporter activity in a middle cerebral artery occlusion (MCAO)-induced ischemia injury rat model. Design: Randomized controlled trial. Methods: In this study, we randomly divided them into three groups. Group I included non-occlusion sham controls (n=10), Group II included non-physical training after MCAO (n=10), and Group III included rats that were subjected to physical training after MCAO (n=10). Rats in the physical training group underwent treadmill training, which began at 24 h after MCAO and continued for 14 consecutive days. The training intensity was gradually increased from 5 m/min on the first day to 12 m/min on day 3, and it was maintained until day 14. Focal cerebral ischemia was examined in adult male Sprague-Dawley rats by using the MCAO model. We determined the functional outcomes for each rat on days 1, 7, and 14. Glutamate transporter-1 (GLT-1) activity in the cortex of rats from all three groups was examined at the end of the experiment. Results: Out result show that MCAO rats exhibited severe neurological deficits on the 1 day, and there was no statistically significant in each groups. We observed that the functional outcomes were improved at days 7 and 14 after middle cerebral artery occlusion, and GLT-1 activity was increased in the physical training group (p<0.05). Conclusions: These results indicated that physical training after focal cerebral ischemia exerts neuroprotective effects against ischemic brain injury by improving motor performance and increasing the levels of GLT-1 activity.