• 한국약용작물학회:학술대회논문집
• /
• 2007.05a
• /
• pp.277-278
• /
• 2007

• 한국약용작물학회:학술대회논문집
• /
• 2008.11a
• /
• pp.133-134
• /
• 2008

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

• Journal of Physiology & Pathology in Korean Medicine
• /
• v.22 no.2
• /
• pp.321-327
• /
• 2008

This study evaluated neuroprotective effects of Yanggyuksanhwa-tang (YST) on global cerebral ischemia of diabetic rats. On primary experiment, diabetic condition in rats was induced by streptozotocin injection. Secondarily, global cerebral ischemia was induced by bilateral occlusion of the common carotid artery with hypotension (BCAO) under the diabetic condition. Then neuroprotective effect of YST was observed with changes of neuronal c-Fos and Bax expressions, and GFAP expression in the brain tissues by using immunohistochemistry. YST treatment was resulted significant decrease of c-Fos expression in CA1 hippocampus induced by BCAO on diabetic rats. YST treatment was resulted significant decrease of Bax expression in CA1 hippocampus induced by BCAO on diabetic rats. YST treatment was resulted significant decrease of c-Fos expression in cerebral cortex and caudoputamen induced by BCAO on diabetic rats. YST treatment was resulted significant decrease of GFAP expression in cerebral cortex induced by BCAO on diabetic rats. These results suggest that YST has effects on neuroprotection against cerebral ischemic damage under diabetic condition. And it is supposed that neuroprotective effect of YST reveals by anti-apoptosis mechanism.

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

• Physical Therapy Korea
• /
• v.17 no.1
• /
• pp.69-76
• /
• 2010

Ischemia that causes stroke induces inflammation of brain cells and apoptosis and as a result, it influences much on the functional part of a man. The needle electrode electrical stimulation (NEES) that combines acupuncture of oriental medicine with electric therapy of western medicine relieves inflammation of cells and has effect on regrowth of nerve tissues. This study was conducted to verify the influence of NEES on the occurrence of c-Fos of cerebrum after applying NEES to the meridian point, Zusanli (ST 36) of a rats with induced ischemia. Global ischemia was induced by using ligation method on common carotid artery of male Sprague Dawley (SD) rats. The ligation was maintained for 5 minutes and then suture was removed for blood reperfusion. After inducing global ischemia, NEES was done to the left and right meridian points of Joksamri of a rat for 30 minutes after 12 hours, 24 hours, and 48 hours. The findings were as follows. 1. In the result of immunohistochemical method, the number of c-Fos immune response cells significantly decreased (P<.05) in NEES group than the control group (GI) that did not get NEES. 2. In the result of western blotting, the occurrence of c-Fos after 24 hours from the inducement of ischemia significantly decreased (P<.05) in NEES group than the control group (GI) that did not get NEES. Therefore, as the effect of NEES was shown highest after 24 hours from the ischemia, it is suspected that NEES would take important role in early treatment after cerebral stroke.

• The Journal of Korean Physical Therapy
• /
• v.13 no.2
• /
• pp.281-292
• /
• 2001

This study was performed to investigate the effect of therapeutic exercise on brain-derived neurotrophic factor manifestation after global brain ischemia in rats. Nine rats with global ischemia were divided at random into two group. In the control group, three rats remained in cage. But, in the end, two rats were alive. In the therapeutic exercise group, six rats remained. The five rats of this group was swam for 30 minutes everyday for a week. The brain-derived neurotrophic factor expression was identified from immunohistochemistry. The results of this study were as follows : 1. In the control group, a little expression of brain-derived neurotrophic factor was observed at cortex and hippocampus layer, but cell body and axon was observed obscurely. 2. In the experimental group, a much expression of brain-derived neurotrophic factor was observed at cortex and hippocampus layer, and cell body and axon was observed clearly. In the neurological examination(beam-walking test). experimental group was obtained higher 1.4 points than control group. BDNF expression was increased by swimming for 30 minutes everyday for a week. Therefore, therapeutic exercise contribute to brain plasticity after brain ischemia.

• The Journal of Korean Medicine
• /
• v.24 no.1
• /
• pp.29-40
• /
• 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.

• The Journal of Korean Medicine
• /
• v.24 no.1
• /
• pp.110-121
• /
• 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.

• The Journal of Korean Medicine
• /
• v.27 no.2 s.66
• /
• pp.1-13
• /
• 2006

Objectives : Ischemic brain injury is a worldwide problem that often causes irreversible brain damage. Moreover, prevention of ischemic brain injury is more important than anything else, since after-effects of stroke significantly threat the quality of life. Jukryukjichul-hwan (JRH) is an oriental medicinal formula for stroke patients in Korea. This study evaluated neuroprotective effects of methanol extract of JRH on global cerebral ischemia in rats. Changes of the pyramidal neurons, Bax and TUNEL immuno-positive neurons in CA1 hippocampus were observed using immunohistochemistry. Methods : Sprague-Dawley Rats were induced with temporal global cerebral ischemia (TGI) by occluding the bilateral common carotid artery with hypotension, The rats were divided into 3 groups. We treated one group with methanol extract of JRH after operation, another group before and after the operation. We observed Bax expressions inducing apoptosis of neurons and TUNEL-positive Pyramidal Neurons as an index of survival and apoptosis of pyramidal neurons in CA1 Hippocampus. Results : JRH treatment before and after TGI inhibited Bax expression in CA1 hippocampus. JRH treatment before and after TGI reduced the cell death of pyramidal neurons in CA1 hippocampus. JRH treatment after TGI reduced the cell death of pyramidal neurons in CA1 hippocampus. JRH treatment before and after TGI reduced TUNEL-positive cells in CA1 hippocampus. Conclusion : These results suggest that JRH has a neuroprotective effect (by anti-apoptosis) against cerebral ischemia.