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CAAT/增强子结合蛋白同源蛋白在高血压全脑缺血大鼠海马区的表达 被引量:2

The expression of CAAT/enhancer-binding protein homologous protein in the hippocampus of hypertensive rats after cerebral ischemia/reperfusion injury
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摘要 目的观察血压正常大鼠和自发性高血压大鼠全脑缺血后海马区CCAAT/增强子结合蛋白同源蛋白(CCAAT/enhancer-binding protein homologous protein,CHOP)的表达变化,探讨其在高血压加重脑缺血神经损伤中的作用。方法分别取血压正常大鼠和自发性高血压大鼠,应用改良的Pulsineli 4血管阻断(4-VO)法制作全脑缺血再灌注模型。分别在脑缺血6、24、48h应用HE染色观察海马区神经细胞形态变化、免疫组织化学法和免疫印迹法检测海马区CHOP表达;在48h应用八臂迷宫检测动物行为学的变化。结果与血压正常脑缺血组比较,高血压脑缺血组各时间点存活神经细胞数量减少,6h和24hCHOP表达增多,48h减少;八臂迷宫检测动物总错误次数、参考记忆错误次数和工作记忆错误次数增多。结论高血压可加重脑缺血后神经损伤,其机制与加重CHOP表达增加有关。 Objective To observe the expression of CAAT/enhancer-binding protein homologous protein (CHOP) in the hippocampus of normal rats and spontaneously hypertensive rats (SHR) so as to explore the mechanism of hypertension in aggravating cerebral ischemia/reperfusion injury. Methods We respectively built global cerebral ischemia model in normal rats and SHR by improved four-vessel occlusion. At 6, 24 and 48 hours after ischemia, changes of neuron pathology were observed by HE staining and CHOP expression was measured by immunohistochemistry and Western blot; behavioral changes of rats were assessed with eight-arm maze 48 hours after ischemia. Results Compared with the cerebral ischemia group of normal rats, the density of survival neurons significantly decreased, CHOP expression significantly increased 6 and 24 hours after ischemia, but decreased at 48 hours in the cerebral ischemia group of SHR. Eight-arm maze test showed that the total error frequences, the reference memory error frequences and the working memory error frequences increased. Conclusion Hypertension may aggravate cerebral ischemia reperfusion injury, which might be related to increasing CHOP over- expression.
出处 《西安交通大学学报(医学版)》 CAS CSCD 北大核心 2013年第3期320-324,共5页 Journal of Xi’an Jiaotong University(Medical Sciences)
基金 河北省自然基金资助项目(No.H2012401007) 河北省卫生厅课题(No.20110527)~~
关键词 高血压 脑缺血再灌注 CAAT 增强子结合蛋白同源蛋白 内质网应激 神经细胞 海马 hypertension cerebral ischemia/reperfusion CA_AT/enhancer-binding protein homologous pro-tein endoplasmic reticulum stress neurons hippocampus
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