• Title/Summary/Keyword: ischemic brain

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Effect of Rhei Rhizoma on Brain Edema Induced by MCAO in Rats (대황(大黃)이 뇌허혈 손상에 의한 뇌부종에 미치는 영향)

  • Kang, Kyung-Hwa;Sohn, Nak-Won;Kim, Bum-Hoi
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.23 no.4
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    • pp.866-871
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    • 2009
  • Brain edema is a major importance in the pathophysiology of CNS injuries including stroke. Ischemic brain edema results from both cytotoxic edema, which is severe in astrocytes at early stage, and vasogenic edema caused by excessive blood-brain barrier (BBB) permeability. The present study was performed to determine the effect of Rhei Rhizoma on brain edema induced by middle cerebral artery occlusion (MCAO) in the rats. The neurological symptom, total infarct volume and edema index caused by MCAO were measured. The changes of Matrix Metalloproteinase-9 (MMP-9) and inducible nitric oxide synthase (iNOS) immunoreactivities were also observed. We found that Rhei Rhizoma extract improved the neurological symptom and attenuated the total infarct volume and brain edema caused by ischemic insult. Rhei Rhizoma extract also attenuated the expression of MMP-9 and iNOS. This results suggest that Rhei Rhizoma has a protective effect on the brain edema caused by ischemic insult.

Effect of Bupleuri Radix on c-Fos and c-Jun Expression in Ischemic Damaged Hippocampus of the Aged BCAO Rats (시호(柴胡)가 뇌허혈유발 노령(老齡) 흰쥐의 해마 c-Fos 및 c-Jun 발현에 미치는 영향)

  • Park, Soon-Il;Oh, Kyung-Hwan;Ryu, Do-Kyun;Han, Chang-Ho;Chung, Sung-Hyun;Shin, Gil-Cho;Lee, Won-Chul;Hwang, Joo-Won
    • The Journal of Internal Korean Medicine
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    • v.26 no.3
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    • pp.533-542
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    • 2005
  • Objectives : In this study, aged BCAO rats were used to observe the effect of Bupleuri Radix on brain ischemic injury because aging is an important factor in storke. Methods : The brain ischemic injury was induced by temporary closing carotids on both sides in a low blood pressure state, and Bupleuri Radix was orally administered to 18 month-old BCAO rats. The ischemic damaged hippocampus and c-Fos and c-Jun expression were analyzed by the immunohistochemical staining. Result and Conclusions : Results are summarized as fellows; 1. The c-Fos expression after inducing a brain ischemic injury in the hippocampus was more inhibited in the experimental group than in the control group. 2. The normalized optical density of c-Fos expression was more reduced in cornu ammonis(CA)1, dentate gyrus(DG) areas in the experimental group than in the control group. 3. The c-Jun expression after inducing a brain ischemic injury in the hippocampus was more inhibited in the experimental group than in the control group. 4. The normalized optical density of c-Jun expression was more reduced in CA1 and DG areas in the experimental group than in the control group.

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Neuroprotective Efects of Gagam-ChongMeong-Tang on Cognitive Function after Ischemic Brain Injury in Rats (허혈성 뇌손상 백서에서 가감총명탕(加減聰明湯)이 인지기능에 미치는 효과)

  • Kim, Kyung-Yoon;Kim, Hyung-Woo;Lee, Sang-Yeong;Cha, Dae-Yeon;Lee, Seok-Jin;Kim, Gye-Yep;Kim, Hang-Jung;Jeong, Hyun-Woo
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.22 no.3
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    • pp.556-561
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    • 2008
  • ChongMyeong-Tang (CMT) have been used clinically to treat patient with amnesia and dementia. In addition, CMT have been also used for examinee to improve learning ability in Korea. This study was designed to investigate the effects of Gagam-ChongMeong-Tang (GCMT) on cognitive dysfunction recovery after ischemic brain injury in rats. Rats were divided into three groups; (1) normal, (2) commercial diet after ischemic brain injury (control), (3) CMT diet after ischemic brain injury (experiment). In our study, we carried out Morris water maze test for cognitive motor behavior test and immunohistochemistry study through the change BDNF in the hippocampus($7^{th},\;14^{th}\;day$). In Morris water maze test, cognitive motor function recovery was significantly increased in the experiment group as compared with control group on $7^{th}\;and\;14^{th}\;day$ day (p<0.01). In immunohistochemistric response of BDNF in the hippocampus, more immune reaction was investigated in the experiment group as compared with control group on $7^{th}\;and\;14^{th}\;day$. Especially more immune reaction was experimented $14^{th}$ day. These results imply that GCMT can play a role in facilitating recovery of cognitive function after ischemic brain injury in rats.

Dihydropyrimidinase related protein-2 expression in focal ischemic rat brain and hypoxia-induced PC 12 cell

  • Chung, Myung-Ah;Kim, Hwa-Jung
    • Proceedings of the PSK Conference
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    • 2003.04a
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    • pp.199.1-199.1
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    • 2003
  • Ischemia-induced changes in protein expression may provide important insights into the mechanisms of cellular damage and their potential recovery. In the present study, to investigate protein patterns changed in ischemic condition, the cortical and striatal tissue samples from the permanent and transient ischemic rat brain obtained by middle cerebral occlusion were analysed by proteomic approchese using 20-PAGE and MALOI-MS. (omitted)

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Effect of BHT-C extract on the infarction in cerebral ischemic rats (BHT-C의 허혈성 뇌졸중 동물에서의 뇌부종 억제효과)

  • Kim, Sung-Yoon;Park, Yong-Ki
    • The Journal of Dong Guk Oriental Medicine
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    • v.11
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    • pp.58-65
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    • 2008
  • Objectives : BHT has been commonly used to treatment of brain disorders in Oriental clinic in Korea. The purpose of this study was to determine the inhibitory effect of modified BHT-C extract on the transient forcal cerebral ischemia in rats. Method : We prepared ischemic rats by the transient middle cerebral artery occlution(MCAO; 90 min occlusion and 144 h reperfusion) in rat brains. BHT-C extract (100 and 200 mg/kg, i.p.) was administered every day after the onset of MCAO until 6 day. Result : BHT-C extract increased survival rate of ischemic rats compared with vehicle-treated rats. BHT-C extract treated rats (100 and 200 mg/kg) were shown a significant reduction in infarct volume compared with vehicle-treated rats. Conclusions : These results suggest that BHT-C extract may contribute to its protective effects in brain ischemia through the reduction of brain infarction.

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Intraventricular Hemorrhage Long after Successful Encephaloduroarterio Synangiosis in Moyamoya Patient

  • Chung, Moon-Young;Park, Young-Seok;Kim, Dong-Seok;Choi, Joong-Uhn
    • Journal of Korean Neurosurgical Society
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    • v.46 no.3
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    • pp.257-260
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    • 2009
  • Intraventricular hemorrhage long after successful encephaloduroarterio synangiosis (EDAS) is very rare. The effect of revascularization surgery for preventing hemorrhagic event of moyamoya disease remains controversial. We report a 17-year-old female with intracerebral hemorrhage and intraventricular hemorrahge 10 years after successful EDAS. Even though cerebral vessels angiography showed good collateral circulations without specific weak points, a cerebral hemorrhage could occur in patient with ischemic type of moyamoya disease long after successful indirect bypass operations. Good collateralization of cerebral angiography or magnetic resonance perfusion image after indirect bypass surgery would ensure against ischemic symptoms, not a hemorrhage. And, thus a life-time follow-up strategy might be necessary even if a good collateral circulation has been established.

Molecular Basis of Neuronal Cell Death Following Neonatal Hypoxic-Ischemic Brain Injury

  • Han, Byung-Hee
    • Proceedings of the PSK Conference
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    • 2003.10a
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    • pp.104-105
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    • 2003
  • Hypoxic-ischemic (H-I) encephalopathy in the prenatal and perinatal period is a major cause of morbidity and mortality and often results in cognitive impairment, seizures, and motor impairment (cerebral palsy). Many studies of neonatal H-I brain injury have utilized the well characterized Levine model in which unilateral carotid ligation is followed by exposure to hypoxia. (omitted)

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The Influence of the Application of NEES to GV20 and L14, on HSP27 and HSP70, after the Ischemic Brain Injury

  • Choi, Jung-Hyun
    • 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.

Matrix Metalloproteinase Inhibitors Attenuate Neuroinflammation Following Focal Cerebral Ischemia in Mice

  • Park, Cheol-Hong;Shin, Tae-Kyeong;Lee, Ho-Youn;Kim, So-Jung;Lee, Won-Suk
    • The Korean Journal of Physiology and Pharmacology
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    • v.15 no.2
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    • pp.115-122
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    • 2011
  • The aim of this study was to investigate whether matrix metalloproteinase (MMP) inhibitors attenuate neuroinflammation in an ischemic brain following photothrombotic cortical ischemia in mice. Male C57BL/6 mice were anesthetized, and Rose Bengal was systemically administered. Permanent focal ischemia was induced in the medial frontal and somatosensory cortices by irradiating the skull with cold white light. MMP inhibitors, such as doxycycline, minocycline, and batimastat, significantly reduced the cerebral infarct size, and the expressions of monocyte chemotactic protein-1 (MCP-1), tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$), and indoleamine 2,3-dioxygenase (IDO). However, they had no effect on the expressions of heme oxygenase-1 and neuroglobin in the ischemic cortex. These results suggest that MMP inhibitors attenuate ischemic brain injury by decreasing the expression levels of MCP-1, TNF-${\alpha}$, and IDO, thereby providing a therapeutic benefit against cerebral ischemia.

Protective Effects of Nueihyuljunbang on LPS Combined PMA Induced Cytotocity in C6 Gilal Cell (LPS와 PMA에 손상된 신경교세포에 대한 뇌혈전방의 방어효과)

  • 서관수;문병순;성강경;임규상;신선호
    • The Journal of Korean Medicine
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    • v.22 no.3
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    • pp.1-10
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    • 2001
  • Objectives : The water extract of Nueihyuljunbang (NHJB) has long been used for treatment of ischemic brain damage in Oriental Medicine. However, little is known about the mechanism by which the water extract of NHJB recovers brain cens from ischemic damage. Methods : To elucidate the protective mechanism on ischemic induced cytotoxicity, we investigated the regulation of lipopolysaccharide (LPS) and phorbol-12-myristate-13-acetate (PMA)-induced inducible nitric oxide synthase (iNOS) expression in C6 glial cells. Results : LPS combined PMA treatment for 72 hours in C6 glial cells markedly induced nitric oxide (NO), but treatment of the cells with the water extract of NHJB decreased dose-dependently nitrite formation. In addition, LPS combined PMA treatment for 72 hours induced severe celt death and lactate dehydrogenase (LDH) release in C6 glial cells. However, treatment of the celts with the water extract of NHJB did not induce significant change compared to control cells. Furthermore, the protective effects of the water extract of NHJB were mimicked by the treatment of NGMMA, a specific inhibitor of NOS. LPS combined PMA induced iNOS activation in C6 glial cells caused chromosomal condensation and fragmentation of the nuclei by caspase activation. The treatment of C6 glial cells with the water extract of NHJB might suppress apoptosis via caspase inhibition by regulation of iNOS expression. Conclusions : From the results, we suggest that the protective effects of the water extract of NHJB against ischemic brain damage may be mediated by regulation of iNOS during ischemic condition.

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