• Journal of Acupuncture Research
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• 제21권4호
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• pp.207-215
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• 2004

Objective : In order to prove the effect of Hirudin Herbal-acupuncture this experimental studies were performed by using rats that had neuronal damage due to the Middle Cerebral Artery Occulsion(MCAO). Methods : Microdialysis probes were implanted into the coordinate of striatum of anesthetized rats which consist of sham-operated 8 rats, MCAO-operated 8 rats and Hirudin Herbal-acupuncture administrated 8 rats before MCAO operating. The Hirudin Herbal-acupuncture(0.5mg/kg) was administrated to rats 30 minutes before having an operation causing the MCAO. The surgical excision lead the cross resected brain to the acute ischemic state. The brain was sliced in 2mm thickness and stained with cresyl violet buffer for the measurement of cerebral infarcted area and volume. Results : Based on the result of the tissue inspection for the cerebral ischemic cell, Hirudin Herbal-acupuncture significantly protect neurocytes. Conclusion : We suggest Hirudin Herbal-acupuncture produces protective effects against the neuronal damage induced by MCAO. Therefore, Hirudin Herbal-acupuncture may prevent delayed neuronal death(DND) in selectively vulnerable focal areas of the brain effectively.

• 동의생리병리학회지
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• 제21권5호
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• pp.1250-1259
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• 2007

Bambusae Caulis in Liquamen(BCL) has been commonly prescribed for stroke patients in the traditional Oriental medicine. So this study is aims to investigate the anti-apoptotic and neuroprotective effects of Bambusae Caulis in Liquamen(BCL) manufactured by different production process on the focal ischemia induced by intraluminal filament insertion in rats. The focal ischemia was induced by intraluminal filament insertion into middle cerebral artery. The animals were divided into four groups (n=15 in each group). The ischemia induced and not treated group : Control group, the ischemia induced and oral medication of the three kinds of BCL : BCL-A group, BCL-B group, BCL-C group. BCL-A was produced by heating at a low temperature$(250^{\circ} C)$ in electric kiln and filtering. BCL-B was produced by heating at a high temperature$(900^{\circ} C{\sim}1,000^{\circ}C)$ in yellow earth kiln and refining and filtering. BCL-C was produced by heating at a low temperature$(400^{\circ} C)$ yellow earth kiln and no refining and filtering. The anti-apoptotic and neuroprotective effects of the oral medication of BCL were observed by Bax, BCL-2, cytochrome c, mGluR5, cresyl violet and ChAT-stain. Our study suggests that BCl-A(was produced by heating at a low temperature in electric kiln and filtering) and BCL-C(was produced by heating at a low temperature in yellow earth kiln and no refining and filtering) show anti-apoptotic and neuroprotective effects on the focal ischemia induced by intraluminal filament insertion in rats and BCL-C is more effective than BCL-A.

• 대한한의학방제학회지
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• 제11권2호
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• pp.159-171
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• 2003

This study was done to investigate effects of SR, CF and AR to angiogenesis of cerebral tissues, protecting damage of cerebral neurons and activating them in cerebral contusion-induced rats. I observed these conclusions as follows ; 1. Observation of VEGF-immunoreactive cells : Groups of administered AR were not meaningful in increasing VEGF-immunoreactive cells for 3 days and 7 days, groups of administered SR meaningfully increased them to control groups in all groups, and groups of administered CF meaningfully increased them to control groups in all groups, too, interestingly, increased double to control group for 7 days. 2. Observation on cerebral neurons by Cresyl violet stain : Dendrites and axons of groups of administered SR, AR for 3 days were clearly observed to control group. Cerebral neurons of groups of administered CF for 3days and 7 days were increased a little, but were not meaningful. In conclusion, AR will be careful of being used in cerebral contusion. CF and SR were effective to activating cerebral hemokinesis by inducing angiogenesis in trauma of tissue, but weakly to protecting trauma of cerebral neurons and activating them. I think more studies will be done in these facts.

• 대한한의학회지
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• 제24권1호
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• pp.29-40
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• 2003

Object : This research was performed to investigate the protective effect of Aurantii Immaturus Fructus against ischemic damage using PC12 cells and global ischemia in gerbils. Methods : To observe the protective effect of Aurantii Immaturus Fructus on ischemia damage, viability and changes in activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase and production of malondialdehyde (MDA) were observed after treating PC12 cells with Aurantii Immaturus Fructus during ischemic insult. Gerbils were divided into three groups : a normal group, a 5-min two-vessel occlusion (2VO) group, and an Aurantii Immaturus Fructus administered after 2VO group. The CCAs were occluded by microclip for 5 minutes. Aurantii Immaturus Fructus was administered orally for 7 days after 2VO. The histological analysis was performed at 7 days after the surgery. For histological analysis, the brain tissue was stained with 1% cresyl violet solution. Results : The results showed that 1. Aurantii Immaturus Fructus had a protective effect against ischemia in the CAI area of the gerbil hippocampus 7 days after 5-minute occlusion, 2. In the hypoxia/reperfusion model using PC12 cells, the Aurantii Immaturus Fructus had a protective effect against ischemia in the dose of $0.2{\;}\mu\textrm{g}/ml,{\;}2{\;}\mu\textrm{g}/ml{\;}and{\;}20{\;}\mu\textrm{g}/ml$ 3. Aurantii Immaturus Fructus increased the activities of glutathione peroxidase and catalase, 4. The activity of superoxide dismutase (SOD) was increased by ischemic damage, which might represent self protection. This study suggests that Aurantii Immaturus Fructus has some neuroprotective effect against neuronal damage following cerebral ischemia in vivo with a widely used experimental model of cerebral ischemia in Mongolian gerbils, and it also has protective effects on a hypoxia/reperfusion cell culture model using PCq2 cells. Conclusions : Aurantii Immaturus Fructus has protective effects against ischemic brain damage at the early stage of ischemia.

• 대한한의학회지
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• 제24권1호
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• pp.110-121
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• 2003

Objective : This research was performed to investigate the protective effect of Angelicae Dahuri Radix against ischemic damage using PC12 cells and global ischemia in gerbils. Methods : To observe the protective effect of Angelicae Dahuri Radix on ischemia damage, viability and changes in activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase and production of malondialdehyde (MDA) were observed after treating PC12 cells with Angelicae Dahuri Radix during ischemic insult. Gerbils were divided into three groups : a normal group, a 5-min two-vessel occlusion (2VO) group, and an Angelicae Dahuri Radix administered after 2VO group. The CCAs were occluded by microclip for 5 minutes. Angelicae Dahuri Radix was administered orally for 7 days after 2VO. The histological analysis was performed at 7 days after surgery. For histological analysis, the brain tissue was stained with 1% cresyl violet solution. Results : 1. Angelicae Dahuri Radix has a protective effect against ischemia in the CA1 area of the gerbil hippocampus 7 days after 5-minute occlusion, 2. In the hypoxia/reperfusion model using PC12 cells, Angelicae Dahuri Radix has a protective effect against ischemia in the dose of $0.2\mu\textrm{g}/ml$, $2\mu\textrm{g}/ml$ and $20\mu\textrm{g}/ml$, 3. Angelicae Dahuri Radix increased the activities of glutathione peroxidase and catalase. 4. The activity of superoxide dismutase (SOD) was increased by ischemic damage, which might represent self protection. This study suggests that Angelicae Dahuri Radix has some neuroprotective effect against neuronal damage following cerebral ischemia in vivo with a widely used experimental model of cerebral ischemia in Mongolian gerbils, and it also has protective effects on a hypoxia/reperfusion cell culture model using PC12 cells. Conclusions : Angelicae Dahuri Radix has protective effects against ischemic brain damage at the early stage of ischemia.

• 대한한의학회지
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• 제22권1호
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• pp.10-21
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• 2001

Objective : This study was performed to investigate the protective effect of Stephania tetrandra(ST) against ischemic brain damage after a middle cerebral artery(MCA) occlusion. The effect was evaluated using histological tests, neurobehavioral tests, and biochemical tests. Methods : Rats(Sprague-Dawley) were divided into four groups : sham operated group, MCA occluded group, post MCA occlusion Stephania tetrandra administrated (7.6mg/l00g) group, and normal group. The MCA was occluded by intraluminal method. Stephania tetrandra was administrated orally twice at 1 and 4 hours after MCA occlusion. The neurobehavioral test was performed at 3, 6, 9 and 24 hours after MCA occlusion by posture reflex test and swimming behavioral test. All groups were sacrificed then. The brain tissues were stained with 2% triphenyl tetrazolium chloride(TTC) or 1 % cresyl violet solution, to examine infarct size, volume and cell number. Tumor necrosis $factor-{\alpha}$ level was measured from sera using Enzyme-Linked Immunoabsorbent Assay(ELISA). The mRNA expression level of inflammatory cytokines and related receptor type I and II, $IL-1{\beta}$, IL-6, and IL-10 6hours after MCA occlusion were also studied by reverse transcriptase polymerase chain reaction(RTPCR). Results : The results showed that : Stephania tetrandra (1) reduced infarct size and total infarct volume by 52.2% compared to the control group; (2) attenuated significantly in neuronal death, which was shown by a decrease in cell number(P<0.01) and size(P<0.01) in the boundary area of the infarction; (3) significantly reduced serum $TNF-{\alpha}$ level, and increased the mRNA level of IL-10 in the cortex region(P<0.01). However, there was no significant effect on motor deficit in swimming behavioral test. Conclusions : In conclusion, Stephania tetrandra has protective effects against ischemic brain damage at the early stage of ischemia.

• 대한한방내과학회지
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• 제30권4호
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• pp.674-684
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• 2009

Objectives : In conditions of brain infarction, irreversible axon damage occurs in the central nerve system (CNS), because gliosis becomes a physical and a mechanical barrier to axonal regeneration. Reactive gliosis induced by ischemic injury such as middle cerebral artery occlusion is involved with up-regulation of GFAP and CD81. This study was undertaken to examine the effect of the Gongjin-dan (GJD) on CD81 and GFAP expression and its pathway in the rat brain following middle cerebral artery occlusion (MCAO). Methods : In order to study ischemic injuries on the brain, infarction was induced by MCAO using insertion of a single nylon thread, through the internal carotid artery, into a middle cerebral artery. Cresyl violet staining, cerebral infarction size measurement, immunohistochemistry and microscopic examination were used to detect the expression of CD81 and GFAP and the effect on the infarct size and pyramidal cell death in the brain of the rat with cerebral infarction induced by MCAO. Also, c-Fos and ERK expression were measured to investigate the signaling pathway after GJD administration in MCAO rats. Results : Measuring the size of cerebral infarction induced by MCAO in the rat after injection of GJD showed the size had decreased. GJD administration showed pyramidal cell death protection in the hippocampus in the MCAO rat. GJD administration decreased GF AP expression in the MCAO rat. GJD administration decreased CD81 expression in the MCAO rat. GJD administration induced up-regulation of c-FOS expression compared with MCAO. GJD administration induced down-regulation of ERK expression compared with MCAO. Conclusion : We observed that GJD could suppress the reactive gliosis, which disturbs the axonal regeneration in the brain of a rat with cerebral infarction after MCAO by controlling the expression of CD81 and GFAP. The effect may be modulated by the regulation of c-Fos and ERK. These results suggest that GJD can be a candidate to regenerate CNS injury.

• The Korean Journal of Physiology and Pharmacology
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• 제14권3호
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• pp.157-161
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• 2010

Heat shock proteins (HSPs) are specifically induced by various forms of stress. Hsp70.1, a member of the hsp70 family is known to play an important role in cytoprotection from stressful insults. However, the functional role of Hsp70 in motor function after spinal cord injury (SCI) is still unclear. To study the role of hsp70.1 in motor recovery following SCI, we assessed locomotor function in hsp70.1 knockout (KO) mice and their wild-type (WT) mice via the Basso, Beattie and Bresnahan (BBB) locomotor rating scale, before and after spinal hemisection at T13 level. We also examined lesion size in the spinal cord using Luxol fast blue/cresyl violet staining. One day after injury, KO and WT mice showed no significant difference in the motor function due to complete paralysis following spinal hemisection. However, when it compared to WT mice, KO mice had significantly delayed and decreased functional outcomes from 4 days up to 21 days after SCI. KO mice also showed significantly greater lesion size in the spinal cord than WT mice showed at 21 days after spinal hemisection. These results suggest that Hsp70 has a protective effect against traumatic SCI and the manipulation of the hsp70.1 gene may help improve the recovery of motor function, thereby enhancing neuroprotection after SCI.

• The Korean Journal of Physiology and Pharmacology
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• 제21권1호
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• pp.125-131
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• 2017

Status epilepticus is the most common serious neurological condition triggered by abnormal electrical activity, leading to severe and widespread cell loss in the brain. Lithium has been one of the main drugs used for the treatment of bipolar disorder for decades, and its anticonvulsant and neuroprotective properties have been described in several neurological disease models. However, the therapeutic mechanisms underlying lithium's actions remain poorly understood. The muscarinic receptor agonist pilocarpine is used to induce status epilepticus, which is followed by hippocampal damage. The present study was designed to investigate the effects of lithium post-treatment on seizure susceptibility and hippocampal neuropathological changes following pilocarpine-induced status epilepticus. Status epilepticus was induced by administration of pilocarpine hydrochloride (320 mg/kg, i.p.) in C57BL/6 mice at 8 weeks of age. Lithium (80 mg/kg, i.p.) was administered 15 minutes after the pilocarpine injection. After the lithium injection, status epilepticus onset time and mortality were recorded. Lithium significantly delayed the onset time of status epilepticus and reduced mortality compared to the vehicle-treated group. Moreover, lithium effectively blocked pilocarpine-induced neuronal death in the hippocampus as estimated by cresyl violet and Fluoro-Jade B staining. However, lithium did not reduce glial activation following pilocarpine-induced status epilepticus. These results suggest that lithium has a neuroprotective effect and would be useful in the treatment of neurological disorders, in particular status epilepticus.

• Journal of Acupuncture Research
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• 제25권1호
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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.