文章摘要
Xian Sun,Chao Liu,Min Qian,Zhenghong Zhao,Jun Guo.[J].南京医科大学学报,2010,(2):132~137
Ceramide from sphingomyelin hydrolysis differentially mediates mitogen-activated protein kinases (MAPKs) activation following cerebral ischemia in rat hippocampal CA1 subregion
  
DOI:10.7655
中文关键词: 
英文关键词: ceramide, cerebral ischemia, extracellular-signal regulated kinase, c-Jun N-terminal protein kinase
基金项目:
作者单位
Xian Sun The Laboratory Center for Basic Medical Sciences, Nanjing Medical University, Nanjing 210029, China
Department of Biochemistry and Molecular Biology, Nanjing Medical University, Nanjing, 210029, China 
Chao Liu The Laboratory Center for Basic Medical Sciences, Nanjing Medical University, Nanjing 210029, China
Department of Biochemistry and Molecular Biology, Nanjing Medical University, Nanjing, 210029, China 
Min Qian The Laboratory Center for Basic Medical Sciences, Nanjing Medical University, Nanjing 210029, China
Department of Biochemistry and Molecular Biology, Nanjing Medical University, Nanjing, 210029, China 
Zhenghong Zhao The Laboratory Center for Basic Medical Sciences, Nanjing Medical University, Nanjing 210029, China
Department of Biochemistry and Molecular Biology, Nanjing Medical University, Nanjing, 210029, China 
Jun Guo The Laboratory Center for Basic Medical Sciences, Nanjing Medical University, Nanjing 210029, China
Department of Biochemistry and Molecular Biology, Nanjing Medical University, Nanjing, 210029, China 
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中文摘要:
      
英文摘要:
      Objective: To explore the role that ceramide plays in the activation of mitogen-activated protein kinases (MAPKs) during cerebral ischemia and reperfusion. Methods: Rats were subjected to ischemia by the four-vessel occlusion (4-VO) method. The sphingomyelinase inhibitor TPCK was administered to the CA1 subregion of the rat hippocampus before inducing ischemia. Western blot was used to examine the activity of extracellular-signal regulated kinase (ERK) and c-Jun N-terminal protein kinase (JNK) using antibodies against ERK, JNK and diphosphorylated ERK and JNK. Results: At 1h reperfusion post-ischemia, JNK reached its peak activity while ERK was undergoing a sharp inactivation (P < 0.05). The level of diphosphorylated JNK was significantly reduced but the sharp inactivation of ERK was visibly reversed (P < 0.05) by the sphingomyelinase inhibitor. Conclusion: The ceramide signaling pathway is up-regulated through sphingomyelin hydrolysis in brain ischemia, promoting JNK activation and suppressing ERK activation, culminating in the ischemic lesion.
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