Inhibiting p38 mitogen-activated protein kinase attenuates cerebral ischemic injury in Swedish mutant amyloid precursor protein transgenic mice

作     者：Liangyu Zou Haiyan Qin Yitao He Heming Huang Yi Lu Xiaofan Chu 

作者机构：Department of NeurologyShenzhen People's HospitalSecond Clinical CollegeJinan UniversityShenzhen 518020Guangdong ProvinceChina 

出 版 物：《Neural Regeneration Research》 (中国神经再生研究（英文版）)

年 卷 期：2012年第7卷第14期

页      面：1088-1094页

核心收录：

学科分类：0710[理学-生物学] 071010[理学-生物化学与分子生物学] 1002[医学-临床医学] 081704[工学-应用化学] 1001[医学-基础医学(可授医学、理学学位)] 07[理学] 08[工学] 0817[工学-化学工程与技术] 

基　　金：supported by the National Natural Science Foundation of China, No. 81171191 Shenzhen Bureau of Science Technology and Information, No. 201002013 Guangdong Province Medical Science Fund, No. A2008601 and Jinan University Scientific Research Foundation for Creation and Cultivation, No. 21609708 

主　　题：cerebral ischemia amyloid precursor protein transgenic Alzheimer's disease p38mitogen-activated protein kinase SB239063 neural regeneration 

摘      要：Cerebral ischemia was induced using photothrombosis 1 hour after intraperitoneal injection of the p38 mitogen-activated protein kinase （MAPK） inhibitor $B239063 into Swedish mutant amyloid precursor protein （APP/SWE） transgenic and non-transgenic mice. The number of surviving neurons in the penumbra was quantified using Nissl staining, and the activity of p38 MAPKs was measured by western blotting. The number of surviving neurons in the penumbra was significantly reduced in APP/SWE transgenic mice compared with non-transgenic controls 7 days after cerebral ischemia, but the activity of p38 MAPKs was significantly elevated compared with the non-ischemic hemisphere in the APP/SWE transgenic mice. SB239063 prevented these changes. The APP/SWE mutation exacerbated ischemic brain injury, and this could be alleviated by inhibiting p38 MAPK activity.