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• W2023354489 startingPage "132" @default.
• W2023354489 abstract "To explore the role that ceramide plays in the activation of mitogen-activated protein kinases (MAPKs) during cerebral ischemia and reperfusion.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.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.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." @default.
• W2023354489 created "2016-06-24" @default.
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• W2023354489 date "2010-03-01" @default.
• W2023354489 modified "2023-09-27" @default.
• W2023354489 title "Ceramide from sphingomyelin hydrolysis differentially mediates mitogen-activated protein kinases (MAPKs) activation following cerebral ischemia in rat hippocampal CA1 subregion" @default.
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• W2023354489 doi "https://doi.org/10.1016/s1674-8301(10)60021-8" @default.
• W2023354489 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3596547" @default.
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