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Influence of edaravone on Notch1 and nuclear factor-kappaB in rats with cerebral ischemia/reperfusion injury

查看全文 作　　者：Yonglong Wang Zhiyou Cai Yong Luo Jiaming [1]Gong 高影响力作者 机构地区：[1]Department of Neurology, First Affiliated Hospital of Chongqing Medical University, Chongqing Key Laboratory of Neurology, Chongqing400016, China高影响力机构 出　　处：《Neural Regeneration Research》索引2008年第3卷第12期,共6页高影响力期刊 摘　　要：BACKGROUND: It has been demonstrated that edaravone has a a neuroprotective role, inhibits free radical increase, and reduces cell apoptosis. The Notch pathway is a key factor in neurogenesis and cellular apoptosis. The proinflammatory transcription factor nuclear factor-kappaB (NF-κB) plays an important role in inflam- mation and oxidation. OBJECTIVE: To observe the influence of edaravone on Notch1 and NF-κB mRNA and protein expression in rats with focal cerebral ischemia/reperfusion injury. DESIGN, TIME AND SETTING: This randomized controlled neural and molecular biology experiment was performed at the Department of Neurology, the First Affiliated Hospital of Chongqing Medical Univer- sity, and the Chongqing Key Laboratory of Neurology between July 2007 and May 2008. MATERIALS: Thirty female Wistar rats were used. Edaravone was purchased from Jiangsu Xiansheng Pharmaceutical Limited Company, China. METHODS: Wistar rats were randomly divided into five groups (n = 6). Thread was inserted into the inter- nal carotid artery of the sham operation group but the middle cerebral artery was not ligated. A focal cerebral ischemia/reperfusion model was established by inserting thread into the right middle cerebral artery. The model rats in the edaravone groups were given tail vein injections of edaravone at 3 mg/kg body weight after ischemia for 2 hours and reperfusion for 12 or 24 hours. Ischemia/reperfusion groups (model group) received intravenous infusion of normal saline at the same volume as the edaravone groups after ischemia for 2 hours and reperfusion for 12 or 24 hours. MAIN OUTCOME MEASURES: The volume of the ischemic region was measured by 2,3,5-triphenyltetrazolium chloride staining. Notch1 and NF-κB protein and mRNA expression were meas- ured by immunohistochemistry and RT-PCR. Protein expression was represented by the absorbance value. RESULTS: Edaravone greatly reduced the focal infarct volume. Notch1 and NF-κB protein and mRNA ex- pression were rapidly upregulated following cerebral ischemia/reperfusion injury in model and edaravone groups compared with the sham operation group (P < 0.01). In addition, edaravone treatment significantly upregulated Notch1 expression but down-regulated NF-κB expression compared with model groups (P < 0.01). CONCLUSION: Edaravone possibly protects brain tissue from ischemia/reperfusion injury by upregulating Notch1 expression and regulating NF-κB expression. 关 键 词：脑缺血 核因素kappaB NOTCH1 依达拉奉 神经保护
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