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. Author manuscript; available in PMC: 2009 Sep 1.
Published in final edited form as: J Cereb Blood Flow Metab. 2009 Feb 25;29(5):873–885. doi: 10.1038/jcbfm.2009.13

Figure 2.

Figure 2

The diagram shows the cell signaling pathways, which were involved in postconditioning. Reperfusion after stroke leads to ROS eruption, which causes dysfunction of the Akt cell signaling pathway, increases δ PKC activity, although decreases ε PKC activity; in addition, ROS also activates JNK and ERK activity. Furthermore, the Akt pathway is associated with the JNK and ERK pathways. The PI3K–Akt inhibition directly results in dephosphorylation of GSK3β and β-catenin degradation, and indirectly causes cytochrome c release and caspase-s activity. ε PKC may activate KATP channel resulting in neuroprotection. ROS, reactive oxygen species; Cyto C, cytochrome c; Cas-3, caspase-3; GSK 3 β, glycogen synthase kinase 3β; PI3K, phosphoinositide 3-kinase; PKC, protein kinase C; P-Akt, phosphorylated Akt; P-PTEN, phosphorylated phosphatase and tensin homolog deleted on chromosome 10; P-PDK1, phosphorylated phosphoinositide-dependent protein kinase-1; JNK, c-Jun N-terminal kinases; ERK, extracellular signal-regulated kinases; KATP channels, ATP-sensitive potassium channels.