• Journal of Nutrition and Health
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• v.36 no.6
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• pp.570-576
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• 2003

The remarkable change of phenomenon induced by stress increase energy metabolism that can induce many reactive oxygen species (ROS) production. ROS can peroxidize cellular macromolecules including lipid and protein. The object of this study was to investigate whether stress may induce cellular damage by producing ROS and whether vitamin E, as a strong lipid-soluble antioxidant, can protect cells against reactive oxygen species produced by noise and immobilization stress in SD rats. The stress group increased 5-hydroxyindole aceti acid (5-HIAA) , one of the stress hormone, in brain tissue and free fatty acid in plasma. Vitamin I treatment had no effect on 5-HIAA but free fatty acid contents decreased with a fortified vitamin I diet. Furthermore, the body weight of vitamin I-treated rats increased more than that of the stress group. Lipid peroxidation and protein degradation as an index of oxidative damage in brain tissue decreased with the use of the fortified vitamin I diet supplement. The results suggest that vitamin I supplements have a protective effect against noise and immobilization stress-induced oxidative damage in brain tissue.

• Journal of Physiology & Pathology in Korean Medicine
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• v.16 no.2
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• pp.245-256
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• 2002

This studt was investigated to prove the effect of SPBST on the hypertension, the thrombosis and the brain damage. The results were as follows; 1. SPBST affected the htpertension as adepressant, but insignificant. 2. SPBST decreased significantly dopamine, aldosterone but ineffective on the epinephrine, norepinephrine and renin activity. 3. SPBST increased the NO product but insignificant. 4. SPBST had a death suppression effect by 50% in pulmonary thrombosis inducement experiment and activated slightly on the fibrinolytic activity. 5. SPBST suppressed significantly platelet diminution and prolonged insignificantly PT and APTT. 6. On the measure of the blood flow rate induced by the thrombus, in vivo SPBST accelerated the blood flow rate, in vitro insignificant. 7. SPBST had no toxicity on the PC12 cell and B103 cell induced by amyloid β protein (-35) and a protective effect, in proportion to the density. 8. SPBST decreased significantly coma duration time in a Infatal dose of KCN and showed 50% of survival rate in a fatal dose. 9. SPBST decreased significantly ischemic area and edema incited by the MCA blood flow block. These results indicate that SPBST can be used in hypertension, the thrombosis, the brain damage, the ischemic cerebral infarction and the acute stage of the brain damage. Further study will be needed about the functional mechanism and etc.

• 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 Physiology & Pathology in Korean Medicine
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• v.17 no.3
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• pp.728-737
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• 2003

This study was investigated to prove the effect of GMGHT on the gultamate receptor, free radical and brain damage in rats sujected to Brain Ischemia The results were as follows; 1, GMGHT showed significant inhibitory effect of GMGHT on LDH release induced by NMDA, AMPA, and kinate. 2. GMGHT showed significant inhibitory effect of GMGHT on LDH release induced by BSO and Fe/sup 2+/. 3. GMGHT decreased coma duration time in a infatal dose of KCN and showed 30% of survival rate in a fatal dose. 4. GMGHT decreased ischemic area and edema incited by the MCA blood flow block. 5. GMGHT showed improvement of forelimb and hindlimb test after MCA occulusion in neurological exemination. 6. GMGHT showed no significant change after MCA occulusion in pathological observation as normal group. These results indicate that GMGHT can be used in the brain damage sujected to Brain Ischemia. Further study will be needed about the functional mechanism and etc.

• Neonatal Medicine
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• v.15 no.1
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• pp.94-99
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• 2008

Although neonatal hypoglycemia is a common metabolic abnormality in newborn infants, brain injuries resulting from isolated neonatal hypoglycemia are rare. Many infants who are hypoglycemic do not exhibit clinical manifestations, while other infants are symptomatic and at risk for permanent brain damage. There is no disagreement that hypoglycemia can cause neonatal encephalopathy and result in permanent brain injury. Occipital brain injury associated with neonatal hypoglycemia can result in long-term disability, epilepsy, and visual impairment. Infants should receive ongoing developmental and visual surveillance for lateonset epilepsy, and visual or cognitive impairment. We report two cases of newborn infants with abnormal visual evoked potentials (VEP) caused by neonatal hypoglycemic encephalopathy.

• Archives of Pharmacal Research
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• v.23 no.4
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• pp.413-417
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• 2000

The effect of ischemia/reperfusion-induced neuronal damage on the memory impairment were investigated using active avoidance and Morris water maze tasks in Wistar rats. Focal ischemia was induced by 1 h occlusion of the right middle cerebral artery (MCA) of Wistar male rats. Reperfusion was induced by releasing the occlusion and restoring the blood circulation for 24 h. The acquisition and preservation memory tested by active avoidance showed a significant difference between the sham and ischemia/reperfusion group. The water maze acquisition performance was also significant difference between sham and ischemia/repefusion groups in both latency and moving distance. The infarction volume was increased by the ischemia/reperfusion. Furthermore, the cresyl violet staining of the ischemia/reperfusion brain showed severe neuronal damage (pyramidal cell loss) in the cortex in addition to the striatum lesion of brain. This study shows that pyramidal cell damage in the cortex lesion may be partially related to memorial disturbance in the ischemia/reperfusion brain injury.

• Proceedings of the PSK Conference
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• 2003.04a
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• pp.200.1-200.1
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• 2003

The purpose of this study is to examine whether an brain to blood efflux system for taurine is present on the blood-brain barrier (BBB) or not and this efflux transport system is regulated by CNS cell damage with oxidative stress agent such as diethyl maleate (DEM) or tumor necrosis factor-a (TNF-${\alpha}$), by using the brain efflux index (BEI) method. The brain efflux index value is defined as the relative amount of test compound efflux from cerebrum compared with that of a reference compound, [$\^$14/C] carboxyinulin, which has limited BBB permeability. (omitted)

• Journal of Korean Neurosurgical Society
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• v.58 no.1
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• pp.22-29
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• 2015

Objective : Perinatal hypoxic-ischemic encephalopathy (HIE) and prolonged febrile seizures (pFS) are common neurologic problems that occur during childhood. However, there is insufficient evidence from experimental studies to conclude that pFS directly induces hippocampal injury. We studied cognitive function and histological changes in a rat model and investigated which among pFS, HIE, or a dual pathologic effect is most detrimental to the health of children. Methods : A rat model of HIE at postnatal day (PD) 7 and a pFS model at PD10 were used. Behavioral and cognitive functions were investigated by means of weekly open field tests from postnatal week (PW) 3 to PW7, and by daily testing with the Morris water maze test at PW8. Pathological changes in the hippocampus were observed in the control, pFS, HIE, and HIE+pFS groups at PW9. Results : The HIE priming group showed a seizure-prone state. The Morris water maze test revealed a decline in cognitive function in the HIE and HIE+pFS groups compared with the pFS and control groups. Additionally, the HIE and HIE+pFS groups showed significant hippocampal neuronal damage, astrogliosis, and volume loss, after maturation. The pFS alone induced minimal hippocampal neuronal damage without astrogliosis or volume loss. Conclusion : Our findings suggest that pFS alone causes no considerable memory or behavioral impairment, or cellular change. In contrast, HIE results in lasting memory impairment and neuronal damage, gliosis, and tissue loss. These findings may contribute to the understanding of the developing brain concerning conditions caused by HIE or pFS.

• Journal of Physiology & Pathology in Korean Medicine
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• v.19 no.4
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• pp.993-999
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• 2005

This research was peformed to investigate protective effect of Sophora Subprostrata fractions against focal ischemic brain damage after middle cerebral artery(MCA) occlusion using intraluminal suture. Rats were divided into six groups: MCA-occluded group(Control): each administered groups with Sophora Subprostrata total phase(Total), Sophora Subprostrata Aqueous phase (Aqueous), Sophora Subprostrata BuOH phase(BuOH), and Sophora Subprostrata Alkaloid phase(Alkaloid) after MCA-occlusion; sham-operated group(Sham). The right MCA was occluded by A poly-L-lysine coated 4-0 nylon suture thread through the internal carotid artery permanently. Sophora Subprostrata and fractions were administered orally(Smg/ml) for 7 days after MCA-occlusion. The Drain tissue was stained with $2\%$ triphenyl tetrazolium chloride on ischemic brain tissue(2mm section). The results showed that 1) Sophora Subprostrata total phase reduced infarct size and total infarct volume compared to the control group at 24 hours after MCA-occlusion, 2) Sophora Subprostrata Aqueous phase reduced infarct size and total infarct volume compared to the control group at 24 hours after MCA-occlusion, 3) Sophora Subprostrata Alkaloid phase reduced infarct size compared to the control group at 24 hours after MCA-occlusion, but 4) at 7 days after MCA-occlusion, Sophora Subprostrata did not show effective recovery compared with control group. Sophora Subprostrata has protective effects against brain damage at the early stage of focal cerebral ischemia. Sophora Subprostrata total and Aqueous phase produced more pronounced protective effect against focal ischemic brain damage.

• Preventive Nutrition and Food Science
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• v.15 no.4
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• pp.255-261
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• 2010

Ischemic stroke, a major cause of death and disability worldwide, is caused by occlusion of cerebral arteries that, coupled with or without reperfusion, results in prolonged ischemia (hypoxia and hypoglycemia) and, ultimately, brain damage. In this study, we examined whether methanol extract of the whole plant of Cassia mimosoides var. nomame Makino that grows naturally in Korea, as well as Japan and China, and some of its fractions obtained by partitioning with organic solvents could protect human hepatocellular carcinoma cells (HepG2) under hypoxic condition by inhibiting apoptosis. We also investigated if these extracts could attenuate brain damage in a rat model of 2 hr of ischemia, generated by middle cerebral artery occlusion, and 22 hr of reperfusion. The whole extract ($100{\mu}g$/mL) maintained the cell number at more than half of that initially plated, even after 24 hr of cell culture under hypoxic condition (3% $O_2$). In the absence of the whole extract, almost all of the cells were dead by this time point. This improvement of cell viability came from a delay of apoptosis, which was confirmed by observing the timing of the formation of a DNA ladder when assessed by gel electrophoresis. Of fractions soluble in hexane, ethyl acetate (EA), butanol and water, EA extracts were selected for the animal experiments, as they improved cell viability at the lowest concentration ($10{\mu}g$/mL). The whole extract (200 mg/kg) and EA extract (10 and 20 mg/kg) significantly reduced infarct size, a measure of brain damage, by 34.7, 33.8 and 45.2.0%, respectively, when assessed by 2,3,5-triphenyl tetrazolium chloride staining. The results suggest that intake of Cassia mimosoides var. nomame Makino might be beneficial for preventing ischemic stroke through inhibition of brain cell apoptosis.