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[PMID]:29353043
[Au] Autor:Tanaka M; Ishihara Y; Mizuno S; Ishida A; Vogel CF; Tsuji M; Yamazaki T; Itoh K
[Ad] Endereço:Laboratory of Molecular Brain Science, Graduate School of Integrated Arts and Sciences, Hiroshima University, Hiroshima, 739-8521, Japan; Laboratory for Pharmacotherapy and Experimental Neurology, Kagawa School of Pharmaceutical Sciences, Tokushima Bunri University, Kagawa, 769-2193, Japan.
[Ti] Título:Progression of vasogenic edema induced by activated microglia under permanent middle cerebral artery occlusion.
[So] Source:Biochem Biophys Res Commun;496(2):582-587, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Brain edema is a severe complication that accompanies ischemic stroke. Increasing evidence shows that inflammatory cytokines impair tight junctions of the blood-brain barrier, suggesting the involvement of microglia in brain edema. In this study, we examined the role of microglia in the progression of ischemic brain edema using mice with permanent middle cerebral artery occlusion. The intensity of T2-weighted imaging (T2WI) in the cerebral cortex and the striatum was elevated 3 h after occlusion and spread to peripheral regions of the ischemic hemisphere. Merged images of 2,3,5-triphenyl tetrazolium chloride staining and T2WI revealed the exact vasogenic edema region, which spread from the ischemic core to outside the ischemic region. Microglia were strongly activated in the ischemic region 3 h after occlusion and, notably, activated microglia were observed in the non-ischemic region 24 h after occlusion. Pretreatment with minocycline, an inhibitor of microglial activation clearly suppressed not only vasogenic edema but also infarct formation. We demonstrated in this study that vasogenic edema spreads from the ischemic core to the peripheral region, which can be elicited, at least in part, by microglial activation induced by ischemia.
[Mh] Termos MeSH primário: Edema Encefálico/etiologia
Encéfalo/patologia
Infarto da Artéria Cerebral Média/complicações
Microglia/patologia
[Mh] Termos MeSH secundário: Animais
Edema Encefálico/patologia
Progressão da Doença
Infarto da Artéria Cerebral Média/patologia
Masculino
Camundongos Endogâmicos ICR
Água/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
059QF0KO0R (Water)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180122
[St] Status:MEDLINE


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[PMID]:29441969
[Au] Autor:Lin S; Wu J; Guo W; Zhu Y
[Ti] Título:Effects of leonurine on intracerebral haemorrhage by attenuation of perihematomal edema and neuroinflammation the JNK pathway.
[So] Source:Pharmazie;71(11):644-650, 2016 11 02.
[Is] ISSN:0031-7144
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Perihematomal edema plays a critical role in secondary brain injury in intracerebral hemorrhage (ICH), which is associated with inflammation, hematoma toxicity and oxidative stress. In this work, we investigated the protective effects of leonurine, an alkaloid of Herbal Leonuri, and possible mechanisms to provide a basis for a new therapeutic approach for ICH treatment. In in vivo studies, we demonstrated for the first time that leonurine treatment substantially decreased perihematomal edema, ameliorated neurobehavioral function deficits, reduced apoptosis and protected injured cerebral tissue after ICH. These benefits appear to be ascribed to leonurine effectively attenuating bloodbrain barrier (BBB) breakdown in vivo, by inhibiting degradation of hemoglobin and alleviating inflammatory mediator release. In this study, BV-2 cells were exposed in vitro to oxyhemoglobin (OxyHb) at a concentration of 10 µM to mimic neuroinflammation after ICH. Consistent with the results of the in vivo study, leonurine significantly inhibited OxyHbinduced inflammatory proteins expression in BV-2 cells, mainly through inhibiting the c-Jun N-terminal kinase (JNK) signaling pathway. This is the first time that leonurine is proved to be capable to protect the injured cerebral tissue after ICH, based on alleviating neuroinflammation and attenuating BBB breakdown to ameliorate perihematomal edema.
[Mh] Termos MeSH primário: Edema Encefálico/tratamento farmacológico
Hemorragia Cerebral/tratamento farmacológico
Encefalite/tratamento farmacológico
Ácido Gálico/análogos & derivados
Hematoma/tratamento farmacológico
Proteínas Proto-Oncogênicas c-jun/efeitos dos fármacos
Transdução de Sinais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Comportamento Animal/efeitos dos fármacos
Barreira Hematoencefálica/efeitos dos fármacos
Água Corporal/metabolismo
Edema Encefálico/patologia
Edema Encefálico/psicologia
Hemorragia Cerebral/psicologia
Encefalite/psicologia
Ácido Gálico/farmacologia
Hematoma/patologia
Hematoma/psicologia
Mediadores da Inflamação/metabolismo
Masculino
Metaloproteinase 9 da Matriz/metabolismo
Oxiemoglobinas/metabolismo
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Inflammation Mediators); 0 (Oxyhemoglobins); 0 (Proto-Oncogene Proteins c-jun); 09Q5W34QDA (leonurine); 632XD903SP (Gallic Acid); EC 3.4.24.35 (Matrix Metalloproteinase 9); EC 3.4.24.35 (Mmp9 protein, rat)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180215
[St] Status:MEDLINE
[do] DOI:10.1691/ph.2016.6692


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[PMID]:29205963
[Au] Autor:Li F; Zhang Y; Ma SL
[Ad] Endereço:School of Forensic Medicine, Henan University of Science and Technology, Luoyang 471003, China.
[Ti] Título:[Relationship between the Expression of α-syn and Neuronal Apoptosis in Brain Cortex of Acute Alcoholism Rats].
[So] Source:Fa Yi Xue Za Zhi;32(6):406-409, 2016 Dec.
[Is] ISSN:1004-5619
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:OBJECTIVES: To observe the changes of expression of α-synuclein (α-syn) and neuronal apoptosis in brain cortex of acute alcoholism rats and to explore the mechanism of the damage caused by ethanol to the neurons. METHODS: The model of acute alcoholism rat was established by 50% alcohol gavage. The α-syn and caspase-3 were detected by immunohistochemical staining and imaging analysis at 1 h, 3 h, 6 h and 12 h after acute alcoholism. The number of positive cell and mean of optical density were detected and the trend change was analyzed. The variance analysis and -test were also performed. RESULTS: The number of α-syn positive cell and average optical density in brain cortex of acute alcoholism rat increased significantly and peaked at 6 hour with a following slight decrease at 12 h, but still higher than the groups at 1 h and 3 h. Within 12 hours after poisoning, the number of caspase-3 positive cell and average optical density in brain cortex of rats gradually increased. CONCLUSIONS: The abnormal aggregation of α-syn caused by brain edema and hypoxia may participate the early stage of neuronal apoptosis in brain cortex after acute alcoholism.
[Mh] Termos MeSH primário: Alcoolismo/patologia
Apoptose
Córtex Cerebral/patologia
Neurônios/patologia
alfa-Sinucleína/metabolismo
[Mh] Termos MeSH secundário: Alcoolismo/metabolismo
Animais
Edema Encefálico/patologia
Caspase 3/metabolismo
Córtex Cerebral/metabolismo
Etanol
Hipóxia/patologia
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (alpha-Synuclein); 3K9958V90M (Ethanol); EC 3.4.22.- (Casp3 protein, rat); EC 3.4.22.- (Caspase 3)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171206
[St] Status:MEDLINE
[do] DOI:10.3969/j.issn.1004-5619.2016.06.002


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[PMID]:29428027
[Au] Autor:Allen CJ; Subhawong TK; Hanna MM; Chelala L; Bullock MR; Schulman CI; Proctor KG
[Ti] Título:Does Vasopressin Exacerbate Cerebral Edema in Patients with Severe Traumatic Brain Injury?
[So] Source:Am Surg;84(1):43-50, 2018 Jan 01.
[Is] ISSN:1555-9823
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Arginine vasopressin (AVP) is often used as an alternative pressor to catecholamines (CATs). However, unlike CATs, AVP is a powerful antidiuretic that could promote edema. We tested the hypothesis that AVP promoted cerebral edema and/or increased requirements for osmotherapy, relative to those who received CATs, for cerebral perfusion pressure (CPP) management after traumatic brain injury (TBI). This is a retrospective review of 286 consecutive TBI patients with intracranial pressure monitoring at a single institution from September 2008 to January 2015. Cerebral edema was quantitated using CT attenuation in prespecified areas of gray and white matter. RESULTS: To maintain CPP >60 mm Hg, 205 patients required no vasopressors, 41 received a single CAT, 12 received AVP, and 28 required both. Those who required no pressors were generally less injured; required less hyperosmolar therapy and less total fluid; and had lower plasma Na, lower intracranial pressure, less edema, and lower mortality (all P < 0.05). Edema; daily mean, minimum, and maximum Na levels; and mortality were similar with AVP versus CATs, but the daily requirement of mannitol and 3 per cent NaCl were reduced by 45 and 35 per cent (both P < 0.05). In patients with TBI who required CPP therapy, AVP reduced the requirements for hyperosmolar therapy and did not delay resolution or increase cerebral edema compared with CATs.
[Mh] Termos MeSH primário: Edema Encefálico/tratamento farmacológico
Lesões Encefálicas Traumáticas/tratamento farmacológico
Circulação Cerebrovascular/efeitos dos fármacos
Vasoconstritores/administração & dosagem
Vasopressinas/administração & dosagem
[Mh] Termos MeSH secundário: Adulto
Edema Encefálico/diagnóstico
Edema Encefálico/etiologia
Edema Encefálico/mortalidade
Lesões Encefálicas Traumáticas/complicações
Lesões Encefálicas Traumáticas/diagnóstico
Lesões Encefálicas Traumáticas/mortalidade
Catecolaminas/uso terapêutico
Feminino
Seres Humanos
Masculino
Meia-Idade
Estudos Retrospectivos
Índices de Gravidade do Trauma
Resultado do Tratamento
Vasoconstritores/efeitos adversos
Vasopressinas/efeitos adversos
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Catecholamines); 0 (Vasoconstrictor Agents); 11000-17-2 (Vasopressins)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180212
[St] Status:MEDLINE


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[PMID]:27770229
[Au] Autor:Nishiyama Y; Kanayama H; Mori H; Tada K; Yamamoto Y; Katsube T; Takeshita H; Kawakami K; Kitagaki H
[Ad] Endereço:Department of Radiology, Shimane University Faculty of Medicine, 89-1 Enya-cho, Izumo-shi, Shimane, 693-8501, Japan.
[Ti] Título:Whole brain analysis of postmortem density changes of grey and white matter on computed tomography by statistical parametric mapping.
[So] Source:Eur Radiol;27(6):2317-2325, 2017 Jun.
[Is] ISSN:1432-1084
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: This study examined the usefulness of statistical parametric mapping (SPM) for investigating postmortem changes on brain computed tomography (CT). METHODS: This retrospective study included 128 patients (23 - 100 years old) without cerebral abnormalities who underwent unenhanced brain CT before and after death. The antemortem CT (AMCT) scans and postmortem CT (PMCT) scans were spatially normalized using our original brain CT template, and postmortem changes of CT values (in Hounsfield units; HU) were analysed by the SPM technique. RESULTS: Compared with AMCT scans, 58.6 % and 98.4 % of PMCT scans showed loss of the cerebral sulci and an unclear grey matter (GM)-white matter (WM) interface, respectively. SPM analysis revealed a significant decrease in cortical GM density within 70 min after death on PMCT scans, suggesting cytotoxic brain oedema. Furthermore, there was a significant increase in the density of the WM, lenticular nucleus and thalamus more than 120 min after death. CONCLUSIONS: The SPM technique demonstrated typical postmortem changes on brain CT scans, and revealed that the unclear GM-WM interface on early PMCT scans is caused by a rapid decrease in cortical GM density combined with a delayed increase in WM density. SPM may be useful for assessment of whole brain postmortem changes. KEY POINTS: • The original brain CT template achieved successful normalization of brain morphology. • Postmortem changes in the brain were independent of sex. • Cortical GM density decreased rapidly after death. • WM and deep GM densities increased following cortical GM density change. • SPM could be useful for assessment of whole brain postmortem changes.
[Mh] Termos MeSH primário: Substância Cinzenta/patologia
Mudanças Depois da Morte
Substância Branca/patologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Autopsia
Encefalopatias/patologia
Edema Encefálico/patologia
Mapeamento Encefálico/métodos
Feminino
Seres Humanos
Masculino
Meia-Idade
Neuroimagem/métodos
Estudos Retrospectivos
Tomografia Computadorizada por Raios X/métodos
Substância Branca/diagnóstico por imagem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180102
[Lr] Data última revisão:
180102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161023
[St] Status:MEDLINE
[do] DOI:10.1007/s00330-016-4633-7


  6 / 13118 MEDLINE  
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[PMID]:27776491
[Au] Autor:Salahuddin N; Mohamed A; Alharbi N; Ansari H; Zaza KJ; Marashly Q; Hussain I; Solaiman O; Wetterberg TV; Maghrabi K
[Ad] Endereço:Adult Critical Care Medicine, King Faisal Specialist Hospital & Research Centre, Riyadh, 11211, Saudi Arabia. nsalahuddin@kfsh.edu.sa.
[Ti] Título:The incidence of increased ICP in ICU patients with non-traumatic coma as diagnosed by ONSD and CT: a prospective cohort study.
[So] Source:BMC Anesthesiol;16(1):106, 2016 10 25.
[Is] ISSN:1471-2253
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Unexplained coma after critical illness can be multifactorial. We evaluated the diagnostic ability of bedside Optic Nerve Sheath Diameter [ONSD] as a screening test for non-traumatic radiographic cerebral edema. METHODS: In a prospective study, mixed medical-surgical intensive care units [ICU] patients with non-traumatic coma [GCS < 9] underwent bedside ultrasonographic ONSD measurements. Non-traumatic radiographic cerebral edema [NTRCE] was defined as > 5 mm midline shift, cisternal, sulcal effacement, or hydrocephalus on CT. RESULTS: NTRCE was identified in 31 of 102 patients [30.4 %]. The area under the ROC curve for detecting radiographic edema by ONSD was 0.785 [95 % CI 0.695-0.874, p <0.001]. ONSD diameter of 0.57 cm was found to be the best cutoff threshold with a sensitivity 84 % and specificity 71 %, AUC 0.785 [95 % CI 0.695-0.874, p <0.001]. Using ONSD as a bedside test increased the post-test odds ratio [OR] for NTRCE by 2.89 times [positive likelihood ratio], whereas post-test OR for NTRCE decreased markedly given a negative ONSD test [ONSD measurement less than 0.57 cm]; negative likelihood ratio 0.22. CONCLUSIONS: The use of ONSD as a bedside test in patients with non-traumatic coma has diagnostic value in identifying patients with non-traumatic radiographic cerebral edema.
[Mh] Termos MeSH primário: Edema Encefálico/fisiopatologia
Coma/diagnóstico por imagem
Hipertensão Intracraniana/epidemiologia
Pressão Intracraniana/fisiologia
Nervo Óptico/diagnóstico por imagem
[Mh] Termos MeSH secundário: Edema Encefálico/complicações
Edema Encefálico/epidemiologia
Coma/fisiopatologia
Feminino
Seres Humanos
Incidência
Unidades de Terapia Intensiva
Hipertensão Intracraniana/complicações
Hipertensão Intracraniana/diagnóstico por imagem
Masculino
Meia-Idade
Estudos Prospectivos
Arábia Saudita/epidemiologia
Tomografia Computadorizada por Raios X
Ultrassonografia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171204
[Lr] Data última revisão:
171204
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE


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[PMID]:28681915
[Au] Autor:Lu H; Ma K; Jin L; Zhu H; Cao R
[Ad] Endereço:Intensive Care Unit of Department of Anesthesiology, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
[Ti] Título:17ß-estradiol rescues damages following traumatic brain injury from molecule to behavior in mice.
[So] Source:J Cell Physiol;233(2):1712-1722, 2018 Feb.
[Is] ISSN:1097-4652
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Traumatic brain injury (TBI) is a public health concern, and causes cognitive dysfunction, emotional disorders, and neurodegeration, as well. The currently available treatments are all symptom-oriented with unsatifying efficacy. It is highly demanded to understand its underlying mechanisms. Controlled cortical impact (CCI) was used to induce TBI in aged female mice subjected to ovariectomy. Brain damages were assessed with neurological severity score, brain infarction and edema. Morris water maze and elevated plus maze were applied to evaluate the levels of anxiety. Apoptosis in the hippocampus was assayed with Fluoro-Jade B staining and TUNEL staining. Western blot was employed to measure the expression of NMDA receptor subunits and phosphorylation of ERK1/2, and biochemical assays were used to estimate oxidative stress. 17beta-Estradiol (E2) was intraperitoneally administered at 10-80 µg/kg once per day for 7 consecutive days before or after CCI. Chronic administration of E2 both before and immediately after CCI conferred neuroprotection, reducing neurological severity score, brain infarction, and edema in TBI mice. Additionally, E2 improved many aspects of deleterious effects of TBI on the hippocampus, including neuronal apoptosis, dysfunction in spatial memory, reduction in NR2B, enhancement of oxidative stress, and activation of ERK1/2 pathway. The present study provides clue for the notion that E2 has therapeutic potential for both prevention and intervention of TBI-induced brain damages.
[Mh] Termos MeSH primário: Comportamento Animal/efeitos dos fármacos
Edema Encefálico/tratamento farmacológico
Infarto Encefálico/tratamento farmacológico
Lesões Encefálicas Traumáticas/tratamento farmacológico
Estradiol/farmacologia
Hipocampo/efeitos dos fármacos
Fármacos Neuroprotetores/farmacologia
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Edema Encefálico/metabolismo
Edema Encefálico/fisiopatologia
Edema Encefálico/psicologia
Infarto Encefálico/metabolismo
Infarto Encefálico/fisiopatologia
Infarto Encefálico/psicologia
Lesões Encefálicas Traumáticas/metabolismo
Lesões Encefálicas Traumáticas/fisiopatologia
Lesões Encefálicas Traumáticas/psicologia
Cognição/efeitos dos fármacos
Citoproteção
Modelos Animais de Doenças
Relação Dose-Resposta a Droga
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Feminino
Hipocampo/metabolismo
Hipocampo/patologia
Hipocampo/fisiopatologia
Aprendizagem em Labirinto/efeitos dos fármacos
Memória/efeitos dos fármacos
Camundongos Endogâmicos C57BL
Degeneração Neural
Ovariectomia
Estresse Oxidativo/efeitos dos fármacos
Fosforilação
Receptores de N-Metil-D-Aspartato/metabolismo
Índice de Gravidade de Doença
Transdução de Sinais/efeitos dos fármacos
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (NR2B NMDA receptor); 0 (Neuroprotective Agents); 0 (Receptors, N-Methyl-D-Aspartate); 4TI98Z838E (Estradiol); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170707
[St] Status:MEDLINE
[do] DOI:10.1002/jcp.26083


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[PMID]:28950851
[Au] Autor:Yu N; Wang Z; Chen Y; Yang J; Lu X; Guo Y; Chen Z; Xu Z
[Ad] Endereço:Acupuncture Research Center, Tianjin University of Traditional Chinese Medicine, Tianjin, 300193, China.
[Ti] Título:The ameliorative effect of bloodletting puncture at hand twelve Jing-well points on cerebral edema induced by permanent middle cerebral ischemia via protecting the tight junctions of the blood-brain barrier.
[So] Source:BMC Complement Altern Med;17(1):470, 2017 Sep 26.
[Is] ISSN:1472-6882
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Cerebral edema, erupting simultaneously with severe ischemic stroke, might lead to increased intracranial pressure, cerebral herniation, and ultimately death. Studies conducted previously by our team have demonstrated the fact that bloodletting puncture at hand twelve Jing-well points (HTWP) could alleviate cerebral edema, which mainly results from the disruption of blood-brain barrier (BBB). The study, therefore, was first designed to demonstrate whether BBB-protection serves an important role in the edema-relief effect of HTWP bloodletting, based on which to research the molecular mechanism underlying. METHODS: The rats were made into model suffering from permanent middle cerebral artery occlusion (pMCAO) and then bloodletting puncture were treated at HTWP once a day. Wet and dry weight method was adopted to evaluate the degree of brain edema, evans blue extravasation and electron microscopy were used to evaluate the integrity of the BBB, and RT-qPCR was carried out to analyze the expression level of occludin, claudin-5, ICAM-1, and VEGF. RESULTS: Results revealed that bloodletting puncture treatment could reduce water content of brain and the permeability of BBB caused by ischemic stroke. In bloodletting puncture group, ameliorated tight junctions could be observed under electron microscopy. It was demonstrated in further study that, in bloodletting group, compared with pMCAO one, the expression levels of occludin and claudin-5 were up-regulated, while ICAM-1 and VEGF were down-regulated. CONCLUSIONS: In conclusion, bloodletting puncture at HTWP might play a significant role in protecting the tight junctions of BBB, thus alleviating cerebral edema induced by ischemic stroke. Therefore, the therapy of bloodletting puncture at HTWP may be a promising strategy for acute ischemic stroke in the future.
[Mh] Termos MeSH primário: Pontos de Acupuntura
Barreira Hematoencefálica/fisiologia
Sangria
Edema Encefálico/terapia
Infarto da Artéria Cerebral Média/terapia
Junções Íntimas/fisiologia
[Mh] Termos MeSH secundário: Animais
Masculino
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171027
[Lr] Data última revisão:
171027
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170928
[St] Status:MEDLINE
[do] DOI:10.1186/s12906-017-1979-6


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[PMID]:28923326
[Au] Autor:Cetin C; Erdogan AM; Dincel GC; Bakar B; Kisa U
[Ad] Endereço:Kirikkale University, Faculty of Medicine, Kirikkale, Turkey.
[Ti] Título:Effects of Sulphasalazine in Cerebral Ischemia Reperfusion Injury in Rat.
[So] Source:Arch Med Res;48(3):247-256, 2017 Apr.
[Is] ISSN:1873-5487
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Management of cerebral ischemia/reperfusion (I/R) injury is still difficult process today. AIMS OF THE STUDY: Aim of present study was to investigate therapeutic properties of sulfasalazine in cerebral transient I/R injury in rat. METHODS: Except Control group (n = 5), 20 Wistar albino rats were allocated for acute and chronic stage investigation of I/R injury, and temporary aneurysm clips were attempted to both internal carotid arteries for thirty min. Four hours later, 40 mg/kg once a day sulfasalazine was administered to animals of SL-A and SL-C groups, orally. Animals were decapitated, following which pyknotic and necrotic neuronal cells, perivascular edema, irregularities of intercellular organization (IIO) of hippocampal regions, and cortical necrotic neurons of parietal lobe were counted or scaled histopathologically. Tissue malonyldialdehyde (MDA), myeloperoxidation (MPO), total nitrite/nitrate (NO), interleukin 1-beta (IL-1ß), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) level values were evaluated biochemically. RESULTS: Sulfasalazine could reduce perivascular edema, IIO, cortical and hippocampal neuronal cell death in both stages. It could decrease MDA in acute stage, but not reduce IL-1ß, IL-6, MPO, NO, and TNFα levels. It could increase IL-1ß levels in chronic stage but not affect to IL-6, MPO, MDA, NO, TNF-α levels. CONCLUSION: Sulfasalazine could improve histopathological architecture of hypoxic tissue in both stages of I/R injury in rat. It could inhibit lipid peroxidation cascades just in acute stage. These results suggested that therapeutic mechanisms of sulfasalazine in cerebral I/R injury should be investigated by using more specific laboratory methods in future studies.
[Mh] Termos MeSH primário: Anti-Inflamatórios não Esteroides/uso terapêutico
Isquemia Encefálica/tratamento farmacológico
Traumatismo por Reperfusão/tratamento farmacológico
Sulfassalazina/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Edema Encefálico/tratamento farmacológico
Edema Encefálico/metabolismo
Isquemia Encefálica/metabolismo
Isquemia Encefálica/patologia
Córtex Cerebral/efeitos dos fármacos
Córtex Cerebral/metabolismo
Córtex Cerebral/patologia
Hipocampo/efeitos dos fármacos
Hipocampo/metabolismo
Hipocampo/patologia
Interleucina-1beta/metabolismo
Interleucina-6/metabolismo
Peroxidação de Lipídeos/efeitos dos fármacos
Masculino
Malondialdeído/metabolismo
Óxido Nítrico/metabolismo
Peroxidase/metabolismo
Ratos Wistar
Traumatismo por Reperfusão/metabolismo
Traumatismo por Reperfusão/patologia
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Interleukin-1beta); 0 (Interleukin-6); 0 (Tumor Necrosis Factor-alpha); 31C4KY9ESH (Nitric Oxide); 3XC8GUZ6CB (Sulfasalazine); 4Y8F71G49Q (Malondialdehyde); EC 1.11.1.7 (Peroxidase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170920
[St] Status:MEDLINE


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[PMID]:28922367
[Au] Autor:Schneider T; Frieling D; Schroeder J; Regelsberger J; Schoen G; Fiehler J; Gellißen S
[Ad] Endereço:Department of Diagnostic and Interventional Neuroradiology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
[Ti] Título:Perihematomal diffusion restriction as a common finding in large intracerebral hemorrhages in the hyperacute phase.
[So] Source:PLoS One;12(9):e0184518, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: There is growing evidence that a perihematomal area of restricted diffusion (PDR) exists in intraparenchymal hemorrhages (IPH) within 1 week of symptom onset (SO). Here, we study characteristics and the clinical impact of the PDR in patients with hyperacute (≤ 6 hours from SO) IPH by means of apparent diffusion coefficient (ADC). METHODS: This monocentric, retrospective study includes 83 patients with first-ever primary IPH from 09/2002-10/2015. 3D volumetric segmentation was performed for the IPH, PDR, and perihematomal edema (PHE) on fluid-attenuated inversion recovery, T2*/susceptibility weighted images, and ADC images. RESULTS: A PDR was seen in 56/83 patients (67.5%) presenting with hyperacute IPH. Multivariate logistic regression analysis revealed every 10-year increase of age (HR 1.929, 95% CI 1.047-3.552, P = .035) and male gender (HR 5.672, 95% CI 1.038-30.992, P = .045) as significant predictors of the presence of a PDR, but not IPH size, IPH location, nor National Institutes of Health Stroke Scale Score (NIHSS) at admission. We found no difference in NIHSS at discharge, hematoma removal, or mortality rate in PDR-positive patients. ADC values of the PDR show a step-wise normalization with increasing time from SO. CONCLUSIONS: Occurrence of a PDR is a common finding in supratentorial hyperacute IPH, but shows no adverse short-term clinical impact. It may represent transient oligemic and metabolic changes.
[Mh] Termos MeSH primário: Edema Encefálico
Hemorragia Cerebral
Imagem por Ressonância Magnética
[Mh] Termos MeSH secundário: Fatores Etários
Idoso
Edema Encefálico/diagnóstico por imagem
Edema Encefálico/mortalidade
Edema Encefálico/fisiopatologia
Edema Encefálico/cirurgia
Hemorragia Cerebral/diagnóstico por imagem
Hemorragia Cerebral/mortalidade
Hemorragia Cerebral/fisiopatologia
Hemorragia Cerebral/cirurgia
Feminino
Seres Humanos
Masculino
Meia-Idade
Estudos Retrospectivos
Fatores de Tempo
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170919
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184518



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