Cyclooxygenase-1 gene knockout does not alter middle cerebral artery occlusion in a mouse stroke model

被引：24

作者：

Cheung, RTF ^{[1
]}

Pei, Z ^{[1
]}

Feng, ZH ^{[1
]}

Zou, LY ^{[1
]}

机构：

[1] Univ Hong Kong, Fac Med, Dept Med, Queen Mary Hosp, Hong Kong, Hong Kong, Peoples R China

来源：

NEUROSCIENCE LETTERS | 2002年 / 330卷 / 01期

关键词：

cyclooxygenase-1; focal cerebral ischemia; mice; infarct volume; gene knockout; triphenyltetrazolium chloride;

D O I：

10.1016/S0304-3940(02)00738-3

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Cyclooxygenase (COX) is crucial in inflammation; COX-1 is constitutional, and COX-2 is inducible. In this study, neurological function and infarct volume were evaluated at 24 h after permanent endovascular middle cerebral artery occlusion (MCAO) in both COX-1-gene knockout (homozygous or heterozygous) and wide-type mice. Similar infarct volumes and neurological deficits were seen among mice of different genotypes. There was no difference among the groups in arterial blood pressure and regional cerebral blood flow during the first 30 min of ischemia. Our results failed to confirm the harmful effect of losing COX-1 activity due to gene knockout in a permanent endovascular MCAO mouse stroke model. (C) 2002 Published by Elsevier Science Ireland Ltd.

引用

页码：57 / 60

页数：4

共 20 条

[1] Middle cerebral artery occlusion in the mouse by intraluminal suture coated with poly-L-lysine: neurological and histological validation [J].

Belayev, L ;

Busto, R ;

Zhao, WZ ;

Femandez, G ;

Ginsberg, MD .

BRAIN RESEARCH, 1999, 833 (02) :181-190

[2] Ischaemic damage of brain microvessels: inherent risks for thrombolytic treatment in stroke [J].

del Zoppo, GJ ;

Von Kummer, R ;

Hamann, GF .

JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY, 1998, 65 (01) :1-9

[3] Cyclooxygenase in biology and disease [J].

Dubois, RN ;

Abramson, SB ;

Crofford, L ;

Gupta, RA ;

Simon, LS ;

Van De Putte, LBA ;

Lipsky, PE .

FASEB JOURNAL, 1998, 12 (12) :1063-1073

[4] Regulation of the cerebral circulation: Role of endothelium and potassium channels [J].

Faraci, FM ;

Heistad, DD .

PHYSIOLOGICAL REVIEWS, 1998, 78 (01) :53-97

[5] Allergic lung responses are increased in prostaglandin H synthase-deficient mice [J].

Gavett, SH ;

Madison, SL ;

Chulada, PC ;

Scarborough, PE ;

Qu, W ;

Boyle, JE ;

Tiano, HF ;

Lee, CA ;

Langenbach, R ;

Roggli, VL ;

Zeldin, DC .

JOURNAL OF CLINICAL INVESTIGATION, 1999, 104 (06) :721-732

[6] The Cycloxygenase-2 inhibitor SC58236 is neuroprotective in an in vivo model of focal ischemia in the rat [J].

Govoni, S ;

Masoero, E ;

Favalli, L ;

Rozza, A ;

Scelsi, R ;

Viappiani, S ;

Buccellati, C ;

Sala, A ;

Folco, G .

NEUROSCIENCE LETTERS, 2001, 303 (02) :91-94

[7] Neuroprotection by aspirin and sodium salicylate through blockade of NF-kappa B activation [J].

Grilli, M ;

Pizzi, M ;

Memo, M ;

Spano, P .

SCIENCE, 1996, 274 (5291) :1383-1385

[8] Increased susceptibility to ischemic brain injury in cyclooxygenase-1-deficient mice [J].

Iadecola, C ;

Sugimoto, K ;

Niwa, K ;

Kazama, K ;

Ross, ME .

JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 2001, 21 (12) :1436-1441

[9] Neuroprotective effects of acetylsalicylic acid in an animal model of focal brain ischemia [J].

Khayyam, N ;

Thavendiranathan, P ;

Carmichael, FJ ;

Kus, B ;

Jay, V ;

Burnham, WM .

NEUROREPORT, 1999, 10 (02) :371-374

[10] Reduced susceptibility to ischemic brain injury and N-methyl-D-aspartate-mediated neurotoxicity in cyclooxygenase-2-deficient mice [J].

Ladecola, C ;

Niwa, K ;

Nogawa, S ;

Zhao, XR ;

Nagayama, M ;

Araki, E ;

Morham, S ;

Ross, ME .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2001, 98 (03) :1294-1299

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