• Title/Summary/Keyword: Brain ischemia

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Effects of Sophora Subprostrata against Focal Cerebral Ischemic Damage by Middle Cerebral Artery Occlusion in Rats (광두근이 백서 중대뇌동맥 폐쇄에 의한 국소뇌허혈손상에 미치는 효과)

  • 이현삼;정혁상;강철훈;손낙원
    • The Journal of Korean Medicine
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    • v.21 no.2
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    • pp.68-78
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    • 2000
  • Objective : This research was performed to investigate protective effects of Sophora subprostrata, against ischemic brain damage after a middle cerebral artery(MCA) occlusion. The effect was estimated using histological test, neurobehavioural test, and biochemical test. Methods : Rats(Sprague-Dawley) were divided into four groups: Sham operated group, MCA occluded group, Sophora subprostrata administrated group after MCA occlusion, and Normal group. The MCA was occluded by intraluminal method. Sophora subprostrata was administrated orally twice(l and 4 hours) after middle cerebral artery occlusion. The neurobeavioural test was performed at 3 hours, 6 hours, 9 hours and 24 hours after the surgery by posture reflex test and swimming behavioural test. All groups were sacrificed at 24 hours after the surgery. The brain tissue was stained with 2% triphenyl tetrazolium chioride(TTC) or 1 % cresyl violet solution, to examine effect of Sophora subprostrata on ischemic brain tissue. The blood samples were obtained from the heart of rats. Tumor necrosis factor-a level was measured from sera using Enzyme-Linked Immunoabsorbent Assay(ELISA). Results : The results showed that (1) Sophora subprostrata reduced infarct size and total infarct volume by 54.8% compared to the control group, (2) that neuronal death, which was shown by decrease in cell number and size, was attenuated significantly in the boundary area of the infarction, (3) that serum $TNF-{\alpha}$ㆍlevel was reduced significantly, and finally, there was significant recovery of motor deficit at 3 hours after MCA occluded by Swimming behavioural test. Conclusions :In conclusion, Sophora subprostrata has protective effects against ischemic brain damage at the early stage of ischemia.

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Brain Death and Kidney Transplantation in Dogs (개의 뇌사와 신장이식)

  • 우흥명;권오경
    • Journal of Veterinary Clinics
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    • v.18 no.4
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    • pp.358-362
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    • 2001
  • Brain dead (BD) patients remain the largest source of solid organs for transplantation. BD has shown to decrease graft function and survival in rodent models. The aim of this study was to evaluate how brain death affects graft viability in the donor and kidney tolerance to cold preservation as assessed by survival in a canine transplantation. 13 Beagle dogs were used for the study. Brain death was induced by the sudden inflation of a subdural balloon catheter with continuous monitoring of arterial blood pressure and eletroencephalographic activity (n=3). Sixteen hours after conformation of brain death, kidney graft were retrieved (n=6). Non-BD donors served as controls (n=4). All kidneys were flushed with University of Wisconsin (UW) solution and preserved for 24 hours at 4$^{\circ}C$ before transplantation. Recipient survival rates, serum creatinine level were analyzed. Brain death induced the well-known Cushing reaction with a severe increase in blood pressure and tachycardia. Thereafter, cardiac function returned progressively to baseline within 8 hours and remained stable until the end of the experiment. All of dogs in both group transplanted were survived until 7 days (100%), and the kidneys showed functional early rejection at 8.3$\pm$0.5 days and 8.5$\pm$0.5 days after transplantation, in BD and allograft group, respectively. BD kidneys were functionally similar to control kidneys for 7 days after transplantated. Brain death has no deleterious effect on preservation injury and survival of dog kidney transplantation, although it induces changes in hemodynamic parameters. This study reveals that kidneys from BD donors do not exhibit more ischemia reperfusion injury, and support good early function and survival.

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Effects of $K^+$ Channel Modulators on Extracellular $K^+$ Accumulation during Ischemia in the Rat Hippocampal Slice (해마절편의 허혈성 $K^+$ 축적에 대한 $K^+$채널 조절 약물의 작용)

  • Choi, Jin-Kyu;Chun, Boe-Gwun;Ryu, Pan-Dong
    • The Korean Journal of Physiology and Pharmacology
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    • v.1 no.6
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    • pp.681-690
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    • 1997
  • Loss of synaptic transmission and accumulation of extracellular $K^+([K^+]_O)$ are the key features in ischemic brain damage. Here, we examined the effects of several $K^+$channel modulators on the early ischemic changes in population spike (PS) and $[K^+]_o$ in the CA1 pyramidal layer of the rat hippocampal slice using electrophysiological techniques. After onset of anoxic aglycemia (AA), orthodromic field potentials decreased and disappeared in $3.3{\pm}0.22\;min$ $(mean{\pm}SEM,\;n=40)$. The hypoxic injury potential (HIP), a transient recovery of PS appeared at $6.0{\pm}0.25\;min$ (n=40) in most slices during AA and lasted for $3.3{\pm}0.43\;min$. $[K^+]_o$ increased initially at a rate of 0.43 mM/min (Phase 1) and later at a much faster rate (12.45 mM/min, Phase 2). The beginning of Phase 2 was invariably coincided with the disappearance of HIP. Among $K^+$ channel modulators tested such as 4-aminopyridine (0.03, 0.3 mM), tetraethylammonium (0.1 mM), NS1619 $(0.3{\sim}10\;{\mu}M)$, niflumic acid (0.1 mM), glibenclamide $(40\;{\mu}M)$, tolbutamide $(300\;{\mu}M)$ and pinacidil $(100\;{\mu}M)$, only 4-aminopyridine (0.3 mM) induced slight increase of $[K^+]_o$ during Phase 1. However, none of the above agents modulated the pattern of Phase 2 in $[K^+]_o$ in response to AA. Taken together, the experimental data suggest that 4-aminopyridine-sensitive $K^+$channels, large conductance $Ca^{2+}-activated$ $K^+$ channels and ATP-sensitive $K^+$ channels may not be the major contributors to the sudden increase of $[K^+]_o$ during the early stage of brain ischemia, suggesting the presence of other routes of $K^+$ efflux during brain ischemia.

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The Effect of Electroacupuncture on Reactive Gliosis Expressing GFAP in Rat with Transient Global Cerebral Ischemia (흰쥐 일과성 뇌허혈 시 GFAP으로 표지되는 반응성 신경아교세포증에 대한 전침의 효과)

  • Cho, Mi-Suk
    • The Journal of the Korea Contents Association
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    • v.11 no.2
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    • pp.341-352
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    • 2011
  • The purpose of this study was carried out to investigate the effect of electroacupuncture on reactive gliosis expressing GFAP in rat with transient global cerebral ischemia. Subjects were randomly divided into two groups, a control group and a electroacupuncture group on ST36, LI11 and SP9 with 2 Hz and 1 mA. The rats were sacrificed on 1, 3 and 7 days after transient cerebral ischemia using ligation of left common carotid artery. After making brain slide sections, they were immunostained with GFAP antisera(1:2,500). The results were as follows: The numbers of astrocytes of electroacupuncture group were decreased than those of control group at every 1, 2 and 7 days. Especially, the numbers of astrocytes at 3 days(p<0.01) and 8 days(p<0.05) were different statistically. And astrocytes had resting, hypertrophic and moving types on cerebral cortex. The decrease of numbers of astrocytes expressing GFAP showed that electroacupuncture could localise and minimize the brain damage by transient cerebral ischemia and cause brain cell plasticity.

The Effect of Modified Boyanghwano-tang on the Brain Infarction Through the Anti-apoptosis of Neuronal Cells in Ischemic Rats (가미보양환오탕이 뇌허혈모델에서 신경세포보호를 통해 뇌경색억제에 미치는 효과)

  • Han, Chang-Ho;Park, Yong-Ki
    • Journal of Acupuncture Research
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    • v.27 no.4
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    • pp.29-38
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    • 2010
  • Objectives : The purpose of the study is to determine the neuroprotective effect of modified Boyanghwano-tang(mBHT), a traditional Korean medicine, on the transient focal cerebral ischemia in rats. Methods : Focal ischemia and reperfusion were induced by middle cerebral artery occlusion(MCAO) for 90 min, followed by 144 h reperfusion in rats. mBHT(200mg/kg body weight, p.o.) was administrated in rats once a day during reperfusion. At the end of treatment, brain infarction was measured by TTC staining, and histological change was observed by H&E staining. The expressions of Bax, Bcl-2 and cytochrome c in ischemic brains were determined by immunofluorescent analysis. Results : mBHT significantly reduced the cerebral infarct volumes of the MCAO rats. mBHT also attenuated the neuronal cell death and the expressions of pro-apoptotic molecules, bax and cytochrome c in ischemic brains. Further, mBHT significantly increased the survival time of ischemeic rats and the expression of anti-apoptotic molecule, Bcl-2 in ischemic brains. Conclusions : Our results suggest that mBHT is neuroprotective and may prove to be useful adjunct in the treatment of ischemic stroke.

Estrogen Regulate Neuroprotection and PDI Gene Expression in Ischemic Rat Brain

  • Yu, Seong-Jin;Kim, Do-Rim;Kim, Jee-Yun;Youm, Mi-Young;Lee, Chae-Kwan;Kang, Sung-Goo
    • Proceedings of the Korean Society of Developmental Biology Conference
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    • 2003.10a
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    • pp.69-69
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    • 2003
  • Neuroprotective strategies have been appeared to be effective in a variety of stroke models. One of the major focuses has been related to the activities of estrogen. $17\beta$-estradiol valerate(EV) has been reported to exert neuroprotective effects when administered before an ischemic insult. The purpose of this study was to determine whether EV can protect against brain injury via estrogen receptor. Chronic and acute pretreatment can reduce the ischemic damage of focal cerebral ischemia in OVX rat, indicating that EV may be a new therapeutic class of drugs to prevent neuronal damage associated with cerebral ischemia. RNAs were extracted from the hippocampus of ovariectomized female rat with or without EV. Differential gene expression profiles were revealed(Bone morphogenetic protein type 1A receptor, Protein disulphide isomerase, cytochrome bc-1 complex core P, thiol-specific antioxidant protein). RT-PCR and in situ hybridization were used to validate the relative expression pattern obtained by the cDNA array. This Study was supported by the Korea Science and Engineering Foundation(KOSEF) through the Biohealth Products Research Center(BPRC), Inje University, Korea

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Chunghyuldan Downregulates the Activation of Transcription Factors NF - kB and AP-1 of BV-2 Cells Induced by Lipopolysaccharide

  • WEE Sung-SooK;BAE Eun-Ah;PARK Jin-Sun;KIM Hee-Sun;CHo Hee Jae;Ryu Jong-Hoon;KIM Dong-Hyun
    • Biomolecules & Therapeutics
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    • v.13 no.4
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    • pp.214-219
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    • 2005
  • Chunghyuldan (Qingxuedan in Chinese) (CHD) has been used for patients with atherosclerosis and brain ischemia in Korea. To evaluate antiischemic activity of CHD, its antiinflammatory effect in lipopolysaccharide-induced BV-2 cells was investigated. CHD potently inhibited nitric oxide (NO) production in LPS-induced BV-2 cells with an $IC_{50}$ value of 4.8${\mu}g/ml$. CHD did not only inhibit mRNA and protein expression levels of inducible NO synthase and cyclooxygenase-2 in LPS-induced BV-2 cells, but also repressed mRNA expression levels of proinflammatory cytokines IL-l$\beta$ and TNF-$\alpha$. CHD also downregulated the activation of NF-kB and AP-l transcription factors induced by LPS. These results suggest that CHD may improve inflammatory brain ischemia by the downregulation the activation of NF-kB and AP-l transcription factors.

Neuroprotective Effects of Hyulbuchookau-tang(血府逐瘀湯) on Global Cerebral Ischemia of the Rats (혈부축어탕(血府逐瘀湯)이 흰쥐의 전뇌허혈에 미치는 영향)

  • Cho, Eun-Hee;Kim, Young-Gyun;Kwon, Jung-Nam
    • The Journal of Korean Medicine
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    • v.28 no.2 s.70
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    • pp.44-53
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    • 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.

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Comparative study on Hsp25 expression in Mongolian gerbil and mouse cerebellum

  • Lee, Heang-Yeon;Kim, Seong-Hwan;Lee, Jae-Bong;Shin, Chang-Ho
    • Korean Journal of Veterinary Service
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    • v.29 no.4
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    • pp.469-482
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    • 2006
  • The term 'heat shock protein (Hsps)' was derived from the fact that these proteins were initially discovered to be induced by hyperthermic conditions. In response to a range of stressful stimuli, including hyperthermia, immobilization, UV radiation, amino acid analogues, arsenite, various chemicals, and drugs the mammalian brain demonstrates a rapid and intense induction of the heat shock protein. Moreover, Hsps were expressed on the various pathological conditions including trauma, focal or global ischemia, hypoxia, infarction, infections, starvation, and anoxia. Especially, Hsp25 has a protective activity, facilitated by the ability of the protein to decrease the intracellular levels of reactive oxygen species (ROS) as well as its chaperone activity, which favors the degradation of oxidized proteins. Recently, it has clearly demonstrated that Hsp25 is constitutively expressed in the adult mouse cerebellum by parasagittal bands of purkinje cells in three distinct regions, the central zone (lobule VI-VII) and nodular zone (lobule IX-X), and paraflocculus. The Mongolian gerbil has been introduced into stroke study model because of its unique brain vasculature. There are no significant connections between the basilarvertebral system and the carotid system. This anatomy feature renders the mongolian gerbil susceptible to forebrain ischemia-induced seizure. The present study is designed to examine the pattern of Hsp25 expression in the cerebellum of this animal in comparison with that in mouse.

The Neuroprotective Effects of Carnosine in Early Stage of Focal Ischemia Rodent Model

  • Park, Hui-Seung;Han, Kyung-Hoon;Shin, Jeoung-A;Park, Joo-Hyun;Song, Kwan-Young;Kim, Doh-Hee
    • Journal of Korean Neurosurgical Society
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    • v.55 no.3
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    • pp.125-130
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    • 2014
  • Objective : This study was conducted to elucidate neuroprotective effect of carnosine in early stage of stroke. Methods : Early stage of rodent stroke model and neuroblastoma chemical hypoxia model was established by middle cerebral artery occlusion and antimycin A. Neuroprotective effect of carnosine was investigated with 100, 250, and 500 mg of carnosine treatment. And antioxidant expression was analyzed by enzyme linked immunosorbent assay (ELISA) and western blot in brain and blood. Results : Intraperitoneal injection of 500 mg carnosine induced significant decrease of infarct volume and expansion of penumbra (p<0.05). The expression of superoxide dismutase (SOD) showed significant increase than in saline group in blood and brain (p<0.05). In the analysis of chemical hypoxia, carnosine induced increase of neuronal cell viability and decrease of reactive oxygen species (ROS) production. Conclusion : Carnosine has neuroprotective property which was related to antioxidant capacity in early stage of stroke. And, the oxidative stress should be considered one of major factor in early ischemic stroke.