• Journal of Physiology & Pathology in Korean Medicine
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• v.16 no.5
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• pp.893-898
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• 2002

Citri Reticulatae Viride Pericarpium extract(CRVP) have been used in oriental medicine for many centuries as a therapeutic agent for smoothing the liver and regulating the circulation of qi, and promoting digestion and removing stagnated food. The effects of CRVP on the inhibition of brain damage in cerebral ischemia is not known. Therefore, this Study was designed to investigate the cerebral protective effects of CRVP on the transient cerebral ischemia using modern techniques, and further to provide the possibility of scientification of oriental medicine. The size of cerebral infarct size was measured by morphometry, and brain edema was measured by morphometry and brain water content determination. The results were a$ follows ; 1. Water fraction of CRVP was reduced infect area of rats brain slices which were subjected to a transient cerebral ischemia in a dose-dependent manner. 2. Methylene chloride fraction and hexane fraction of CRVP was significantly reduced infarct area of rats brain slices which were subjected to a transient cerebral ischemia in a dose-dependent manner. 3. Methylene chloride fraction and hexane fraction of CRVP was significantly reduced infarct volume of rats brain which was subjected to a transient cerebral ischemia in a dose-dependent manner. 4. Methylene Chloride fraction and hexane fraction of CRVP was significantly decreased brain edema induced by a transient cerebral ischemia in a dose-dependent manner. 5. Methylene chloride fraction and hexane fraction of CRVP was significantly decreased brain water content of rats which were subjected to a transient cerebral ischemia. It is suggested that CRVP has an anti-ischemic effect through the inhibition of brain damage in a transient cerebral ischemia, and that in future further development of main effective constituent in CRVP can provide a novel therapeutic strategy for cerebral ischemia.

• The Journal of Korean Medicine
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• v.26 no.3 s.63
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• pp.146-161
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• 2005

Objectives : This study investigated neuroprotective effects of Polygoni Multiflori Radix on cerebral ischemia of hyperlipidemic rats. Methods : Effects of Polygoni Multiflori Radix were evaluated with changes of infarct size after He focal cerebral ischemia induced by the middle cerebral artery occlusion, changes of pyramidal neurons and expressions of Bax and Bcl-2 apoptosis regulating factors after global cerebral ischemia, and changes of serum lipid revels after cerebral ischemia. Results & Conclusions : Results obtained were as follows; 1. Polygoni Multiflori Radix did net reduce the focal cerebral infarct size induced by the middle cerebral artery occlusion under both hyperlipidemic and normal-lipid conditions. 2. Polygoni Multiflori Radix significantly reduced the increase of neuronal cell death in CAl region of hippocampus induced by the global cerebral ischemia under both hyperlipidemic and normal-lipid conditions. 3. Polygoni Multiflori Radix significantly reduced the increase of Bax expression in the CAl region of the hippocampus induced by global cerebral ischemia under both hyperlipidemic and normal-lipid conditions. 4. Polygoni Multiflori Radix significantly increased Bc1-2 expression in the CA1 region of the hippocampus after global cerebral ischemia under normal-lipid condition, but was not effective on that under hyperlipidemic condition. 5. Polygoni Multiflori Radix was not effective on serum total-cholesterol, HDL-cholesterol, LDL-cholesterol and triglyceride levels under normal-lipid conditions, irrespective of focal cerebral infarct or global cerebral ischemia. 6. Polygoni Multiflori Radix significantly reduced the increase of serum total-cholesterol and triglyceride levels, and increased serum LDL-cholesterol level under hyperlipidemic conditions, irrespective of foc31 cerebral infarct or global cerebral ischemia.

• The Journal of Korean Medicine
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• v.23 no.3
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• pp.134-144
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• 2002

Objective : The purpose of this study was to investigate the effect of Jukryuk and Saengkang-juices on cerebral vascular ischemia (CVI) of the middle cerebral artery (MCA). Method : By admiuistration Jukryuk and Saengkang-juices, we compared treated groups with untreated groups, in view of five points as follows: 1) cerebral damage; 2) damaged area of ischemia; 3) cerebral edema; 4) the number of neuronal cells adjacent to the areas damaged by ischemia; and 5) the number of neuronal cells adjacent to the areas damaged by ischemia Results : In this experiment, the effect of Jukryuk and Saengkang-juices was determined by inducing cerebral vascular ischemia after occluding the middle cerebral artery (MCA) in mice, and making observations and comparisons such as alterations in damaged areas and neuronal cellular changes in the brain. Conclusions : According to the above results, Jukryuk and Saengkang-juices can protect the cerebral vascular ischemia.

• Biomolecules & Therapeutics
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• v.7 no.3
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• pp.234-241
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• 1999

The present study assessed the cerebroprotective effect of platelet-activating factor(PAF) antagonists in transient cerebral ischemia of rats. Right middle cerebral artery (MCA) of Sprague-Dawley rats was occluded for 2 hours using an intraluminal filament technique, and was reperfused for 6 hours following cerebral ischemia. The infarct area of seven coronal brain slices was measured morphometrically following stain ing in the 2% 2,3,5-triphenyltetrazolium chloride solution. The changes in regional cerebral blood flow (rCBF) and pial arteriolar diameter were measured by laser-Doppler flowmetry and by a videomicroscopy, respectively. The infarct size was significantly reduced by PAF antagonists, BN 52021 and CV-6209, which were administered i.p. 10 min before MCA occlusion. Pretreatment with PAF antagonists significantly restored the changes in pial arterial diameter as well as those in rCBF during the period of cerebral ischemia-reperfusion. PAF antagonists significantly inhibited the inducible nitric oxide synthase activity in the pial arteries ipsilateral to ischemia. These results suggest that PAF antagonists exert a cerebroprotective effect against ischemic brain damage through an improvement of postocclusive cerebral blood flow.

• The Journal of Korean Medicine
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• v.39 no.4
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• pp.1-15
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• 2018

Objectives: Cerebral ischemia results from a variety of causes that cerebral blood flow is reduced due to a transient or permanent occlusion of cerebral arteries. Reactive astrocytes and microglial activation plays an important role in the neuronal cell death during ischemic insult. Acupunctural treatment is effective for symptom improvement in cerebrovascular accident, including cerebral ischemia. Methods: In the present study, the effects of acupuncture at the ST40 acupoint on short-term memory and apoptosis in the hippocampal CA1 region following transient global cerebral ischemia were investigated using gerbils. Transient global ischemia was induced by occlusion of both common carotid arteries with aneurysm clips for 5 min. Acupuncture stimulation was conducted once daily for 7 consecutive days, starting one day after surgery. Results: In the present results, ischemia induction deteriorated short term memory, increased apoptosis, and induced reactive astrocyte and microglial activation. Acupuncture at ST40 acupoint ameliorated ischemia-induced short-term memory impairment by suppressing apoptosis in the hippocampus through down-regulation of reactive astrocytes and microglial activation. Conclusion: The present study suggests that acupuncture at the ST40 acupoint can be used for treatment of patients with cerebral stroke.

• The Korea Journal of Herbology
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• v.28 no.2
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• pp.1-7
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• 2013

Objectives : Sesamin, a major lignan in sesame seeds, has been reported to have neuroprotective effects against in vitro ischemia and in vivo MCAo-reperfusion cerebral ischemia model, however, there is no reports in an in vivo global cerebral ischemia model. The purpose of the study was to investigate the neuroprotective effect of sesamin in global cerebral ischemia induced by four-vessel occlusion (4-VO) in rats through inhibition of microglial activation in this model. Methods : The neuroprotective effects were investigated using a 10 min of 4-VO ischemia rat model by measuring intact pyramidal neurons in the CA1 region of the hippocampus using Nissle staining. The antiinflammatory or reducing neurotoxicity effect was investigated using immunohistochemisty, RT-PCR and western blot analysis of inflammatory or neurotoxic mediators. Results : Intraperitoneal injection of sesamin at doses of 0.3, 1.0, 3.0, and 10.0 mg/kg at 0 min and 90 min after ischemia conferred 26.6%, 30.1%, 42.5%, and 30.5% neuroprotection, respectively, compared to the vehicle-treated control group. A 3.0 mg/kg dose of sesamin inhibited microglia activation and consequently, cyclooxygenase-2, inducible nitric oxide, and interleukine-$1{\beta}$ expressions at 48 h after reperfusion. Conclusions : Sesamin protects neuronal cell death through inhibition of microglial activation or the production of neurotoxic metabolites and proinflammatory mediators by microglia such as COX-2, iNOS and IL-$1{\beta}$ in global cerebral ischemia.

• The Journal of Korean Medicine
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• v.30 no.6
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• pp.53-68
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• 2009

Objectives: This study demonstrates the neurological effects of Bojungikki-tang and Bojungikki-tang-gamibang on the focal cerebral ischemia of rats with ischemic damage caused by middle cerebral artery occlusion (MCAO). Methods: Rats were treated with Bojungikki-tang and Bojungikki-tang-gamibang extracts for about five days after MCAO, and the size and volume of cerebral infarction and the ratio of cerebral edema were observed. From the immunohistochemical view, significant changes of outbreak of Bax, Bcl-2, c-Fos, HSP72, and iNOS were observed in the brain tissues. Results: Bojungikki-tang repressed only brain edema and iNOS revelation led by focal cerebral ischemia, when considering significance. In contrast, Bojungikki-tang-gamibang demonstrated significant suppression of cerebral infarction, brain edema, Bax, c-Fos, HSP72, and iNOS induced by focal cerebral ischemia. Conclusions: Bojungikki-tang is considered functional treatment for cerebral ischemic damage; it can be effective to relieve secondary brain edema and immune response. Bojungikki-tang-gamibang can have a direct function to alleviate brain infarct and to control the natural death of nerve cells which cerebral ischemic damage brings about.

• Journal of Korean Neurosurgical Society
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• v.41 no.1
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• pp.30-38
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• 2007

Objective : To elucidate the role of aquaporin-4[AQP4] in cerebral edema formation, we studied the expression and subcellular localization of AQP4 in astrocytes after focal cerebral ischemia. Methods : Cerebral ischemia were induced by permanent middle cerebral artery[MCA] occlusion in rats and estimated by the discoloration after triphenyltetrazolium chloride[TTC] immersion. Change of AQP4 expression were evaluated using western blot. Localization of AQP4 was assessed by confocal microscopy and its interaction with ${\alpha}-syntrophin$ was analyzed by immunoprecipitation. Results : After right MCA occlusion, the size of infarct and number of apoptotic cells increased with time. The ratio of GluR1/GluR2 expression also increased during ischemia. The polarized localization of AQP4 in the endfeet of astrocytes contacting with ventricles, vessels and pia mater was changed into the diffuse distribution in cytoplasm. The interactions of AQP4 and Kir with ${\alpha}-syntrophin$, an adaptor of dystrophin complex, were disrupted by cerebral ischemia. Conclusion : The deranged spatial buffering function of astrocytes due to mislocalized AQP4/Kir4.1 channel as well as increased assembly of $Ca^{2+}$ permeable AMPA receptors might contribute to the development of edema formation and the excitotoxic neuronal cell death during ischemia.

• YAKHAK HOEJI
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• v.43 no.2
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• pp.251-262
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• 1999

In order to investigate pharmacological properties of New Wonbang Woohwangchungsimwon Pill (NSCH) and Wonbang Woohwangchungsimwon Pill (SCH), the effects of NSCH and SCH 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 preventive effects of NSCH and SCH treatments with ischemia-induced brain damage. The ATP in brain tissue was decreased in vehicle-treated ischemic gerbils. This decrease was prevented by SCH treatment. In contrast to what was inhibited by NSCH and SCH treatments. While NSCH and SCH had no effects on the hexobarbital-induced sleeping time, they prevented the seizures induced by electric shock and strychnine. NSCH and SCH showed sedative effect in rotarod and spontaneous activity test. Furthermore, NSCH and SCH showed anti-stress effect. Our findings suggest that the pharmacological profiles of NSCH on cerebral ischemia and central nervous system are similar to those of SCH.

• The Journal of Korean Medicine
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• v.21 no.1
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• pp.11-19
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• 2000

The present study was carried out to investigate the effects of Woowhangcheongshim-won(WCW) on the extracellular concentrations of amino acid neurotransmitters(glutamate, aspartate, GABA, glycine, taurine, alanine, and tyrosine) and organic acid (lactate and pyruvate) in striatum and cerebral infarction volume in rats subjected to permanent focal cerebral ischemia induced by 2 hours of middle cerebral artery occlusion(MCAO), using intracerebral microdialysis as the sampling technique, Microdialysis probes were inserted into the lateral part of the caudate-putamen 2 hours before the experiment and microdialyzates were collected at 20min intervals and analyzed by high performance liquid chromatography, WCW significantly decreased the infarction volume with reducing focal cerebral ischemia-induced increase of extracellular glutamate, asparate, and tyrosine. On the other hand, the increase of GABA and taurine was enhanced after treatment of WCW in the ischemia-induced rats, These results suggest that WCW can produce a neuroprotective effect against cerebral ischemia by regulating extracellular excitatory and inhibitory amino acid levels in relation to the concept of excitotoxicity in brain ischemia.