• The Journal of Korean Medicine
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• v.30 no.1
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• pp.64-75
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• 2009

Objective: This study was designed to investigate the effect of Samultang (SMT) under hippocampus cells ischemia both in vitro and in vivo. Methods: In the in vitro study, HT22 cells, predominantly detected in the cytoplasm, which coincides with the location of the mitochondria, were used as indicators. In the in vivo study, permanent middle cerebral artery occlusion (MCAO) was induced on rats. SMT was given orally 2 h before induction of permanent focal brain ischemic injury. Result: In the in vitro study, SMT had protective effects in glutamate-induced cytotoxicity, which was revealed as apoptosis characterized by chromatic condensation and the loss of mitochondrial membrane potential in HT22 cells. In the in vivo study, TTC (2,3,5-triphenyltetrazolium chloride) staining showed a marked ischemic injury in blood supply territory of the middle cerebral artery (MCA) such as the cerebral cortex and striatum. However, treatment with SMT significantly reduced infarcted volume. SMT increased marked survival of HT22 cells against glutamate-induced cytotoxicity in MTT assay. Conclusion: These results suggest that water extract of SMT provides neuroprotection against ischemic or oxidative injury by inhibition of apoptotic cell death.

• Korean Journal of Veterinary Research
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• v.64 no.1
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• pp.2.1-2.8
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• 2024

This study was performed to assess the antiapoptotic effect of canine platelet-rich plasma (PRP) treated on the canine adipose-derived mesenchymal stem cells (cMSCs) under cold ischemic conditions. The effect of preventing apoptosis of cMSCs was evaluated in the apoptotic condition induced by cold ischemic injury in vitro. To determine the progression of apoptosis, the changes in cell nucleus were observed using 4',6-diamidino-2-phenylindole (DAPI) fluorescence staining. In addition, we examined the mitochondrial membrane potential (MMP) and caspase-3 activity. When the cold hypoxic injury was applied to cMSCs, the apoptotic change was observed by DAPI staining, mitochondrial staining for MMP, and caspase-3 assay. PRP significantly decreased the number of apoptotic cells. Nuclear shrinkage and fragmentation of apoptotic cells in control groups were observed by DAPI staining. The MMP was recovered by the treatment of PRP. In addition, when the luminescence intensity was measured for caspase-3 activity, the value was significantly higher in the PRP treated groups than the control groups. The results of this study showed that the PRP may have a beneficial effect on apoptosis induced by cold ischemic injury.

• The Journal of Korean Medicine
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• v.24 no.3
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• pp.72-83
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• 2003

Objective : The goal of the present study was to investigate the protective effect of Gamiheechum-tang (Jiaweixiqian-tang; GHCT) on brain tissue damage from chemical or ischemic insults. Methods : Levels of cultured cortical neuron death caused by toxic chemicals were measured by LDH release assay. Neuroprotective effects of GHCT on brain tissues were examined in vivo by ischemic model of middle cerebral artery (MCA) occlusion. Results : Animal groups treated with GBCT showed significantly decreased hypertension, and reduced levels of aldosterone, dopamine, and epinephrine in the plasma. GHCT treatments ($l0-200\mu\textrm{g}/ml$) significantly decreased cultured cortical neuron death mediated by AMPA, kainate, BSO, or Fe2+ when measured by LDH release assay. Yet, cell death mediated by NMDA was effectively protected by GHCT at the highest concentration examined ($200\mu\textrm{g}/ml$). In the in vivo experiment examining brain damage by MCA occlusion, affected brain areas by ischemic damage and edema were significantly less in animal groups administered with GHCT compared to the non-treated control group. Neurological examinations of forelimbs and hindlimbs showed that GHCT treatment improved animals' recovery from ischemic injury. Moreover, the extent of injury in cortical and hippocampal pyramidal neurons in ischemic rats was much reduced by GHCT, whose morphological features were similarly observed in non-ischemic animals. Conclusion : The present data suggest that GBCT may play an important role in protecting brain tissues from chemical or ischemic injuries.

• Clinical and Experimental Pediatrics
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• v.64 no.12
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• pp.608-618
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• 2021

Hypoxic-ischemic encephalopathy (HIE) is the most common cause of neonatal encephalopathy with a global incidence of approximately 1 to 8 per 1,000 live births. Neonatal encephalopathy can cause neurodevelopmental and cognitive impairments in survivors of hypoxic-ischemic insults with and without functional motor deficits. Normal neurodevelopmental outcomes in early childhood do not preclude cognitive and behavioral difficulties in late childhood and adolescence because cognitive functions are not yet fully developed at this early age. Therapeutic hypothermia has been shown to significantly reduced death and severe disabilities in term newborns with HIE. However, children treated with hypothermia therapy remain at risk for cognitive impairments and follow-up is necessary throughout late childhood and adolescence. Novel adjunctive neuroprotective therapies combined with therapeutic hypothermia may enhance the survival and neurodevelopmental outcomes of infants with HIE. The extent and severity of brain injury on magnetic resonance imaging might predict neurodevelopmental outcomes and lead to targeted interven tions in children with a history of neonatal encephalopathy. We provide a summary of the long-term cognitive outcomes in late childhood and adolescence in children with a history of HIE and the association between pattern of brain injury and neurodevelopmental outcomes.

• Journal of Oriental Neuropsychiatry
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• v.17 no.3
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• pp.45-56
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• 2006

Objective: Yukmijibwang-Tang(UJT) has been used for Dementia derived by deficiency of Kidney-Yin in the oriental medicine. This study was planned to examine the effects of UJT on the memory loss induced by focal brain ischemic injury in the rats. Methods : Experimental groups were divided into 4 groups ; Normal group, Control group, UJT1 group and UJT2 group. Control group were no treated after focal brain ischemic injury. UJT1 group were administered UJT 0.3 $m{\ell}/kg$ to focal brain ischemic injuried rats for 21 days, UJT2 group were administered UJT 1.2 $m{\ell}/kg$ to focal brain ischemic injuried rats for 21 days. The present author observed the number of errors on the eight-arm radial maze task, the rate of correct choice on the eight-arm radial maze task, the values of density of Cresy1 violet- stained sections in the hippocampal CA1 and the values of density of Acetlycholine Esterase (AchE)stained nuclei in the hippocampal CA1. Results : The number of errors in the Eigth-arm radial maze task was significantly decreased in UJT1 group on 1, 2, 3, 5, 6days, And it was significantly decreased in UJT2 group on 1-6days compared with control group. The rate of correct choice in the eight-arm radial maze task was significantly increased in UJT1, UJT2 group compared with control group. The values of density of Cresyl violet-stained stained sections in the hippocampal CA1 were significantly increased in UJT1, UJT2 group compared with control group. The values of density of AchE in the hippocampal CA1 were increased in UJT1, UJT2 group compared with control group, but the values were not significant. Conclusions: The present author thought that Yukmijihwang-Tang could he used for curing dementia induced by focal brain ischemic injury.

• BMB Reports
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• v.56 no.4
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• pp.234-239
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• 2023

Thioredoxin-like protein 1 (TXNL1), one of the thioredoxin superfamily known as redox-regulator, plays an essential in maintaining cell survival via various antioxidant and anti-apoptotic mechanisms. It is well known that relationship between ischemia and oxidative stress, however, the role of TXNL1 protein in ischemic damage has not been fully investigated. In the present study, we aimed to determine the protective role of TXNL1 against on ischemic injury in vitro and in vivo using cell permeable Tat-TXNL1 fusion protein. Transduced Tat-TXNL1 inhibited ROS production and cell death in H₂O₂-exposed hippocampal neuronal (HT-22) cells and modulated MAPKs and Akt activation, and pro-apoptotic protein expression levels in the cells. In an ischemia animal model, Tat-TXNL1 markedly decreased hippocampal neuronal cell death and the activation of astrocytes and microglia. These findings indicate that cell permeable Tat-TXNL1 protects against oxidative stress in vitro and in vivo ischemic animal model. Therefore, we suggest Tat-TXNL1 can be a potential therapeutic protein for ischemic injury.

• The Journal of the Korea Contents Association
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• v.11 no.4
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• pp.273-282
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• 2011

This study was to investigate the effect of improve forelimb sensorimotor function and neurotrophic factor(GAP-43) expression when differing an application time of tDCS in ischemic brain injury rat model(pre, $1^{st}$, $7^{th}$, $14^{th}$). Focal ischemic brain injury was induced in 80 Sprague-Dawley rats through middle cerebral artery occlusion(MCAO) by 'Longa' method. And then experimental groups were randomly divided into four groups; GroupI: MCAO induction, GroupII: application of tDCS(10 min) after MCAO induction, GroupIII: application of tDCS(20 min) after MCAO induction, GroupIV: application of tDCS(30 min) after MCAO induction. Modified limb placing test and single pellet reaching test were performed to test forelimb sensorimotor function. And the histological examination was also observed through the immunohistochemistric response of GAP-43(growth-associated protein-43) in the cerebral cortex. In modified limb placing test, groupIII(p<0.05) showed significantly improve than the other groups on $14^{th}$). day. In single pellet reaching test, groupIII(p<0.01) and groupIV(p<0.05) significantly improved on $14^{th}$) day. And in immunohistochemistric response of GAP-43, group III showed significantly positive response than the other groups on $14^{th}$ day. These results suggest that the intensity(0.1 mA)/time(20 min) condition of tDCS application has a significant impact on the sensorimotor functional recovery in focal ischemic brain injury rat models.

• Therapeutic Science for Rehabilitation
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• v.7 no.1
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• pp.11-26
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• 2018

Objective : This case study was to verify effects of cognitive rehabilitation and swallowing rehabilitation on Hypoxic-Ischemic Brain Injury patient by Suicidal Attempt. Methods : The subject was a 32-year old Hypoxic-ischemic brain injury patient by suicidal attempt. He received treatment once a day five times a week, for a half an hour for each session from September 8th to December 16th, 2016. Treatment were cognitive and swallowing rehabilitation. He was assessed based on Mini-Mental State Examination-Korean (MMSE-K), Korean-Modified Barthel Index (K-MBI), Computerized Neurocognitive Function Test (CNT), Videofluoroscopic Dysphagia Scale (VDS), American Speech-Language-Hearing Association National Outcomes Measurements System (ASHA-NOMS). Results : The patient's total MMSE-K score increased from 25 to 27. His K-MBI score increased from 74 to 88. His memory, attention span, and executive function (DST, VST, SWCT, WCST) by CNT scores were improved. VDS score has no changes to 34, 44.5 and 34. ASHA-NOMS score also has no change to 6, 2 and 6. Conclusion : The study showed that the application of the treatment of cognitive and swallowing in hypoxic-ischemic brain injury patient by suicidal attempt results has positive effects on cognitive functions, and swallowing function.

• Maxillofacial Plastic and Reconstructive Surgery
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• v.28 no.4
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• pp.287-294
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• 2006

Vascular thrombosis and ischemic necrosis still remain the most significant threats to the survival of free flaps. To date, neutrophils have been implicated in the pathogenesis of postischemic injury. Several studies have demonstrated that modulating the neutrophil response to ischemia-reperfusion injury can decrease the extent of the injury. In addition, some authors noticed that mast cell counts were also increased in flaps exposed to state of ischemia/reperfusion. So, we designed to evaluate the role of mast cells in ischemia/reperfusion by blocking histamine and to compare the effect of L-arginine, a nitric oxide precursor which is known to prevent neutrophil-mediated tissue injury. Epigastric island skin flaps were elevated in 30 rats and rendered ischemic. Thirty minutes prior to reperfusion, the rats were treated with intraperitoneal saline, diphenhydramine, cimetidine, and L-arginine. The necrosis rate of flap at 7 days, the number of neutrophils and mast cells at 20 hours were evaluated. In conclusion, histamine receptor blockers as well as L-arginine significantly decreased flap necrosis in a rat skin island ischemia-reperfusion flap model, but the protective effect was not significantly different in both agent groups.

• Journal of Physiology & Pathology in Korean Medicine
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• v.26 no.5
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• pp.657-664
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• 2012

The aim of this study is to investigate the effects of onion vinegar on the cerebral blood flow by measuring the changes of regional cerebral blood flow (rCBF) and mean arterial blood pressure (MABP) and by observing the recovery of focal ischemic brain injury in rats. Rats are divided into thee groups depending on the medication; control group (no medication), 8.8-OV group (vinegar using 8.8 brix onion medication), 14.6-OV group (vinegar using 14.6 brix onion medication). The medication of onion vinegar significantly increased rCBF but decreased MABP. This result suggests that onion vinegar significantly increased rCBF by dilating arterial diameter. In addition, focal ischemic brain injury is induced in rats by middle cerebral arterial occlusion. The recovery from focal ischemic brain injury is more significantly improved in the groups using onion vinegar compared to the control group. The amount of recovery is measured by the GAP-43 and the medication of onion vinegar significantly increased GAP-43. This result suggests that onion vinegar is effective on the nerve regeneration. After the medication, the change of body weight, outcomes of renal and liver function test, and outcomes of CBC are analysed for safety examination. There are no statistical differences among control group and all experimental groups in the body weight, renal and liver function test, and CBC. In conclusion, these results suggest that onion vinegar can increase rCBF in normal state, and improve the stability of rCBF in ischemic state.