• Journal of Yeungnam Medical Science
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• v.12 no.2
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• pp.260-268
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• 1995

Ischemia results when the decrease in tissue perfusion exceeds the tissues ability to increase an oxygen extraction from the blood. Brain edema has been defined as an abnormal accumulation of fluid within brain parenchyma associated with a volumetric enlargement of the brain tissue. In most instances, the labelling of edema as vasogenic or cytotoxic is only relative. For cerebral protection, there were many possible techniques which could increase or maintain cerebral perfusion and reduce cerebral metabolic demand for oxygen. This study was carried out the effect of mild brain hypothermia which was induced by infusion with cold saline into the carotid artery, during brief episodes of transient global ischemia on postischemic brain edema in rabbit. Eight rabbits were anesthetized with halothane and mechanically ventilated with oxygen. For isolated cerebral perfusion, polyethylene catheter was inserted left carotid artery for infusion of cold saline, external carotid artery was ligated, vertebral arteries were cautherized, right carotid artery was snared for ischemia and femoral artery and vein were also canulated for monitoring and drug treatment. At 3 hours After transient global ischemia, specific gravity of cerebral cortex and hippocampus was compared with no-perfusion group , perfusion with cold saline group and normal group. There was no significant differences in physiologic variables among the groups before transient global ischemia. But during transient global ischemia, brain temperature of perfusion group was decreased when compared to no perfusion group. Specific gravity of cerebral cortex and hippocampus of no-perfusion group and perfusion group was statistically significant when compared to normal group (p<0.01). The results of this study suggested that mild brain hypothermia with intracarotid cold saline infusion during brief episodes of transient global ischemia had decreased postischemic brain edema in rabbit.

• 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.

• YAKHAK HOEJI
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• v.44 no.4
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• pp.371-377
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• 2000

In order to investigate the pharmacological properties of fractions of Astragali Radix and Polygalae Radix, the effects of the fractions on cerebral ischemia and subsequent reperfusion were studied. Brain ischemia was induced by bilateral common carotid artery occlusion in mongolian gerbil. Brains were recirculated for 30 mins after the 20 min occlusion. Methanol and butanol fractions of Astragali Radix and Polygalae Radix were administered orally 2 hrs before common carotid artery occlusion. Histological observations showed that brain ischemia induced severe brain damage evidenced by the presence of necrotic foci, edema and hemorrhage. This injury was prevented by the methanol fraction and butanol fraction of Polygalae Radix. The level of ATP in brain tissue significantly decreased in ischemic gerbils. This decrease was prevented by the pretreatment with butanol fraction of Polygalae Radix. In contrast, the levels of lactate and lipid peroxide were both elevated in ischemic gerbils. This elevation was inhibited by the pretreatments with methanol fraction and butanol fraction of Polygalae Radix. Our findings suggest that the Polygalae Radix improves ischemia-induced brain damage.

• Journal of Physiology & Pathology in Korean Medicine
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• v.18 no.6
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• pp.1777-1783
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• 2004

This study was conducted to determine the effects Wonjiseokchangpo-san on brain damage in transient focal cerebral ischemia. Rats were used for testing in the following three models: Morris Water Maze, Eight-Arm Radial Maze, and Histochemistry. In the Morris Water Maze Model, the Wonjiseokchangpo-san group showed significant decrease in the 3rd and 6th training session compared with the ischemia group. A retention test, in the Morris Water Maze Model, was performed on the 7th day without the escape platform. The Wonjiseokchangpo-san group showed significant increase compared to the ischemia group. In the Eight-Arm radial Maze model, the Wonjiseokchangpo-san group showed significant decrease in the error rate compared to the ischemia group. In the density of hippocampal CA1 cell of the cresyl violet-stained section, the Wonjiseokahangpo-san group showed significant increase compared to the ischemia group. These results suggest that Wonjiseokchangpo-san may have a significant protective effect on brain damage and cognitive dysfunction in transient focal cerebral ischemia.

• The Journal of Korean Medicine
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• v.26 no.2 s.62
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• pp.52-62
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• 2005

Objectives: This study was conducted to determine the effects of Geupunggibodan on brain damage in transient focal cerebral ischemia in rats. Methods: Rats were used for testing in the following three models: Morris water maze, eight-ann radial maze, and histochemistry. Results: In the Morris water maze model, the Geupunggibodan group showed significant decrease in the 3rd, 4th and 6th training sessions compared with the ischemia, group. A retention test in the Morris water maze model was performed on the 7th day without the escape platform. The Geupunggibodan group showed significant increase compared to the ischemia group. In the eight-ann radial maze model, the Geupunggibodan group showed significant decrease in the error rate compared to the ischemia group. In the density of hippocampal CA1 cell of the cresyl violet-stained section, the Geupunggibodan group showed significant increase compared to the ischemia group. Conclusions: These results suggest that Geupunggibodan may have a significant protective effect on brain damage and cognitive dysfunction in transient focal cerebral ischemia.

• Parasites, Hosts and Diseases
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• v.58 no.4
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• pp.461-466
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• 2020

Toxoplasma gondii is an obligate intracellular protozoan parasite that can invade various organs in the host body, including the central nervous system. Chronic intracranial T. gondii is known to be associated with neuroprotection against neurodegenerative diseases through interaction with host brain cells in various ways. The present study investigated the neuroprotective effects of chronic T. gondii infection in mice with cerebral ischemia experimentally produced by middle cerebral artery occlusion (MCAO) surgery. The neurobehavioral effects of cerebral ischemia were assessed by measurement of Garcia score and Rotarod behavior tests. The volume of brain ischemia was measured by triphenyltetrazolium chloride staining. The expression levels of related genes and proteins were determined. After cerebral ischemia, corrected infarction volume was significantly reduced in T. gondii infected mice, and their neurobehavioral function was significantly better than that of the uninfection control group. Chronic T. gondii infection induced the expression of hypoxia-inducible factor 1-alpha (HIF-1α) in the brain before MCAO. T. gondii infection also increased the expression of vascular endothelial growth factor after the cerebral ischemia. It is suggested that chronic intracerebral infection of T. gondii may be a potential preconditioning strategy to reduce neural deficits associated with cerebral ischemia and induce brain ischemic tolerance through the regulation of HIF-1α expression.

• Journal of International Academy of Physical Therapy Research
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• v.2 no.2
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• pp.281-287
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• 2011

This research was attempted to seek for a positive approach within the framework of physical therapy instead of the drug treatment in the past, with regard to the ischemic brain injury in the early stage. Accordingly, the aim of this research is to observe the change of HSP27 and HSP70, the genes that are expressed in the early stage of brain injury and to investigate the effects of needle electrode electrical stimulation(NEES), upon applying NEES after ischemia. The experimental method is to give rise to global ischemia and apply NEES to 27 SD-Pat rats with the particulars of being eight-week-old, male, around 300g, and adapted to laboratory environment for more than a week, and divide them into three groups, that is, GV20 NEES group(n=9), L14 NEES group(n=9), no applied NEES global ischemia(GI) group(n=9), and then observe their changes of HSP27 and HSP70 at the time lapse of 6, 9 hr and 12 hr after ischemia, using immunohistochemistry methods. Upon observing through the immunohistochemistry method, it was noticed that there was a significant difference between the GV20 NEES group and the L14 NEES group as for HSP27 and there were significant differences among all groups as for HSP70(p<.05). Accordingly, it is supposed that the application of NEES after the outbreak of cerebral ischemia delay the apoptosis in the early ischemic part of forebrain or protect neurons against apoptosis.

• Biomolecules & Therapeutics
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• v.25 no.2
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• pp.149-157
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• 2017

The interleukin-1 receptor antagonist (IL-1RA) is a potential stroke treatment candidate. Intranasal delivery is a novel method thereby a therapeutic protein can be penetrated into the brain parenchyma by bypassing the blood-brain barrier. Thus, this study tested whether intranasal IL-1RA can provide neuroprotection and brain penetration in transient cerebral ischemia. In male Sprague-Dawley rats, focal cerebral ischemia was induced by middle cerebral artery occlusion (MCAO) for 1 h. The rats simultaneously received 50 mg/kg human IL-1RA through the intranasal (IN group) or intraperitoneal route (IP group). The other rats were given 0.5 mL/kg normal saline (EC group). Neurobehavioral function, infarct size, and the concentration of the administered human IL-1RA in the brain tissue were assessed. In addition, the cellular distribution of intranasal IL-1RA in the brain and its effect on proinflammatory cytokines expression were evaluated. Intranasal IL-1RA improved neurological deficit and reduced infarct size until 7 days after MCAO (p<0.05). The concentrations of the human IL-1RA in the brain tissue 24 h after MCAO were significantly greater in the IN group than in the IP group (p<0.05). The human IL-1RA was confirmed to be co-localized with neuron and microglia. Furthermore, the IN group had lower expression of $interleukin-1{\beta}$ and tumor necrosis $factor-{\alpha}$ at 6 h after MCAO than the EC group (p<0.05). These results suggest that intranasal IL-1RA can reach the brain parenchyma more efficiently and provide superior neuroprotection in the transient focal cerebral ischemia.

• The Journal of Internal Korean Medicine
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• v.33 no.4
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• pp.572-586
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• 2012

Objectives : This study was designed to investigate the effects of Sasim-tang (SST) on proinflammatory cytokine production in a photothrombotic ischemia mouse model. Methods : Photothrombotic ischemia was induced in stereotactically held male Balb/c mice using rose bengal (10 mg/kg) and cold light. The target of photothrombotic ischemic lesion was 1 mm anterior to bregma and 3 mm lateral to midline with 2 mm in diameter, which are decreased by oral administration of SST. Results : SST protected ischemic death of brain cells through inhibition of pro-inflammatory cytokines production and catalytic activation of caspase-3 protease in photothrombotic ischemia mouse model. Conclusions : The results of this study suggest that SST can have protective effects on brain cell damage in a photothrombotic ischemia mouse model.

• Molecules and Cells
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• v.22 no.1
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• pp.8-12
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• 2006

Neuron-derived orphan receptor (NOR-1) is a member of the thyroid/steroid receptor superfamily that was originally identified in forebrain neuronal cells undergoing apoptosis. In addition to apoptotic stimuli, activation of several signal transduction pathways including direct neuronal depolarization regulates the expression of NOR-1. In this study we tested whether the expression of NOR-1 is changed following transient ischemic injury in the adult rat brain. NOR-1 mRNA increased rapidly in the dentate gyrus of the hippocampal formation and piriform cortex 3 h after transient global ischemia and returned to basal level at 6 h. On the other hand, oxygen-glucose deprivation of cultured cerebral cortical neurons did not alter the expression of NOR-1. These results suggest that expression of NOR-1 is differentially regulated in different brain regions in response to globally applied brain ischemia, but that hypoxia is not sufficient to induce its expression.