作者: Tsutomu Sasaki , Kazuo Kitagawa , Kanato Yamagata , Takako Takemiya , Shigeru Tanaka
DOI: 10.1097/01.WCB.0000100065.36077.4A
关键词:
摘要: Several studies have suggested that cyclooxygenase-2 (COX-2) plays a role in ischemic neuronal death. Genetic disruption of COX-2 has been shown to reduce susceptibility focal injury and N-methyl-d-aspartate-mediated neurotoxicity. The purpose this study was examine the effects deficiency on vulnerability after transient forebrain ischemia. Marked upregulation immunostaining neurons observed at early stage prominent staining persisted CA1 medial sector CA2 over 3 days immunohistologic pattern these sectors gradually condensed perinuclear location. degree hippocampal produced by global ischemia COX-2-deficient mice less than wild-type mice, coincident with attenuation DNA fragmentation hippocampus. Also, treatment selective inhibitor, nimesulide, decreased damages. These results genetic chemical inhibition show ameliorates death mice.