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Conference Paper: Deficiency of COX-1 gene expression in mice reduces the infarction volume in a 24-hour permanent focal cerebral ischemia model

TitleDeficiency of COX-1 gene expression in mice reduces the infarction volume in a 24-hour permanent focal cerebral ischemia model
Authors
Keywordscyclooxygenase
MCAO
knockout
Issue Date2001
PublisherSociety for Neuroscience. The Journal's web site is located at http://sfn.scholarone.com/
Citation
Neuroscience 2001, San Diego, CA, 10-15 November 2001, Presentation no. 329.9 How to Cite?
AbstractInflammatory reactions have an important role in the ischemic pathophysiology. Cyclooxygenase (COX) is the key enzyme in converting arachidonic acid to prostanoids that, in turn, are the major contributors to the intrinsic inflammatory response. In this study, we used COX-1-null mice to investigate the role of COX-1 gene expression in a permanent focal cerebral ischemia model. Adult littermates (wild type +/+, heterozygous +/-, and homozygous -/-), were used. Genetic status was determined using a PCR analysis. The mice were anesthetized with chloral hydrate (350 mg/kg, IP). Right femoral artery was cannulated for monitoring of arterial blood pressure and heart rate. Rectal temperature was kept normal throughout anesthesia. Cerebral blood flow was monitored by Laser-Doppler Flowmetry. Permanent focal cerebral ischemia was achieved by passing a monofilament suture via the right external and internal carotid arteries to occlude the right middle cerebral artery (MCA) at its origin. Mice were killed by decapitation at 24 hours after MCA occlusion. The brains were cut into 2-mm coronal slices for staining with 2% tetrazolium chloride to reveal the infarct. The infarction volume was quantified using computer-assisted image analysis. Relative infarction volumes were, in mean ?SEM, 42.67 ?3.72% (n=6) in COX-1 +/+ mice, 25.97 ?8.48% (n=6) in COX-1 +/- mice, and 28.13 ?6.22% (n=6) in COX-1 -/- mice, respectively. There was no significant difference in physiological parameters and cerebral perfusion among the groups. Our results demonstrated that lack of COX-1 gene expression might reduce infarction volume in a 24-hour permanent MCA occlusion model in mice.
Persistent Identifierhttp://hdl.handle.net/10722/54112

 

DC FieldValueLanguage
dc.contributor.authorPei, Zen_HK
dc.contributor.authorFeng, ZHen_HK
dc.contributor.authorCheung, RTFen_HK
dc.date.accessioned2009-04-03T07:37:06Z-
dc.date.available2009-04-03T07:37:06Z-
dc.date.issued2001en_HK
dc.identifier.citationNeuroscience 2001, San Diego, CA, 10-15 November 2001, Presentation no. 329.9en_HK
dc.identifier.urihttp://hdl.handle.net/10722/54112-
dc.description.abstractInflammatory reactions have an important role in the ischemic pathophysiology. Cyclooxygenase (COX) is the key enzyme in converting arachidonic acid to prostanoids that, in turn, are the major contributors to the intrinsic inflammatory response. In this study, we used COX-1-null mice to investigate the role of COX-1 gene expression in a permanent focal cerebral ischemia model. Adult littermates (wild type +/+, heterozygous +/-, and homozygous -/-), were used. Genetic status was determined using a PCR analysis. The mice were anesthetized with chloral hydrate (350 mg/kg, IP). Right femoral artery was cannulated for monitoring of arterial blood pressure and heart rate. Rectal temperature was kept normal throughout anesthesia. Cerebral blood flow was monitored by Laser-Doppler Flowmetry. Permanent focal cerebral ischemia was achieved by passing a monofilament suture via the right external and internal carotid arteries to occlude the right middle cerebral artery (MCA) at its origin. Mice were killed by decapitation at 24 hours after MCA occlusion. The brains were cut into 2-mm coronal slices for staining with 2% tetrazolium chloride to reveal the infarct. The infarction volume was quantified using computer-assisted image analysis. Relative infarction volumes were, in mean ?SEM, 42.67 ?3.72% (n=6) in COX-1 +/+ mice, 25.97 ?8.48% (n=6) in COX-1 +/- mice, and 28.13 ?6.22% (n=6) in COX-1 -/- mice, respectively. There was no significant difference in physiological parameters and cerebral perfusion among the groups. Our results demonstrated that lack of COX-1 gene expression might reduce infarction volume in a 24-hour permanent MCA occlusion model in mice.-
dc.languageengen_HK
dc.publisherSociety for Neuroscience. The Journal's web site is located at http://sfn.scholarone.com/en_HK
dc.relation.ispartofSociety for Neuroscience Annual Meeting-
dc.rightsSociety for Neuroscience Abstract viewer & itinerary planner. Copyright © Society for Neuroscience.en_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectcyclooxygenase-
dc.subjectMCAO-
dc.subjectknockout-
dc.titleDeficiency of COX-1 gene expression in mice reduces the infarction volume in a 24-hour permanent focal cerebral ischemia modelen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailFeng, ZH: zhfeng@hku.hken_HK
dc.identifier.emailCheung, RTF: rtcheung@hku.hken_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.hkuros115198-

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