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Ceramide from sphingomyelin hydrolysis differentially mediates mitogen-activated protein kinases (MAPKs) activation following cerebral ischemia in rat hippocampal CA1 subregion
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The work was supported by grants from the National Natural Science Foundation of China (No.30871200) and the Practice and Innovation Training Program for Students in Colleges and Universities of Jiangsu Province (NO.20090370).

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    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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Xian Sun, Chao Liu, Min Qian, Zhenghong Zhao, Jun Guo.[J].南京医科大学学报(自然科学版),2010,(2):132-137

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