Neural Regeneration Research ›› 2012, Vol. 7 ›› Issue (14): 1088-1109.

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

Liangyu Zou, Haiyan Qin, Yitao He, Heming Huang, Yi Lu, Xiaofan Chu   

  1. Department of Neurology, Shenzhen People’s Hospital, Second Clinical College, Jinan University, Shenzhen 518020, Guangdong Province, China
  • Received:2012-01-06 Revised:2012-03-08 Online:2012-05-15 Published:2012-05-15
  • Contact: Xiaofan Chu, M.D., Ph. D., Professor, Department of Neurology, Shenzhen People’s Hospital, Second Clinical College, Jinan University, Shenzhen 518020, Guangdong Province, China cxf987@tom.com
  • About author:Liangyu Zou☆, M.D., Ph.D., Chief physician, Department of Neurology, Shenzhen People’s Hospital, Second Clinical College, Jinan University, Shenzhen 518020, Guangdong Province, China

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Abstract:

Cerebral ischemia was induced using photothrombosis 1 hour after intraperitoneal injection of the p38 mitogen-activated protein kinase (MAPK) inhibitor SB239063 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.

Key words: cerebral ischemia, amyloid precursor protein, transgenic, Alzheimer’s disease, p38 mito-gen-activated protein kinase, SB239063, neural regeneration