Fig. 1. Investigated signaling components in isoflurane postconditioning in the infarct-remodeled rat heart. Protein kinase B (PKB)/Akt is downstream of phosphatidylinositol 3-kinase (PI3K), a key enzyme in the reperfusion injury salvage kinase cascade (  full arrows ). Phosphorylated PKB/Akt activates 70-kd ribosomal protein S6 kinase (p70S6K) and endothelial nitric oxide synthase (eNOS) and inactivates glycogen synthase kinase 3β (GSK3β) by phosphorylation. Activation of protein kinase C ϵ (PKC-ϵ), p38 mitogen-activated protein kinase (p38 MAPK), and extracellular signal–regulated protein kinases (ERKs), potentially involved in cardioprotection from reperfusion injury (  dashed arrows ), were also assessed. LY294002: specific inhibitor of PI3K. 

Fig. 1. Investigated signaling components in isoflurane postconditioning in the infarct-remodeled rat heart. Protein kinase B (PKB)/Akt is downstream of phosphatidylinositol 3-kinase (PI3K), a key enzyme in the reperfusion injury salvage kinase cascade (  full arrows ). Phosphorylated PKB/Akt activates 70-kd ribosomal protein S6 kinase (p70S6K) and endothelial nitric oxide synthase (eNOS) and inactivates glycogen synthase kinase 3β (GSK3β) by phosphorylation. Activation of protein kinase C ϵ (PKC-ϵ), p38 mitogen-activated protein kinase (p38 MAPK), and extracellular signal–regulated protein kinases (ERKs), potentially involved in cardioprotection from reperfusion injury (  dashed arrows ), were also assessed. LY294002: specific inhibitor of PI3K. 

Close Modal

or Create an Account

Close Modal
Close Modal