Effects of wortmannin on phosphorylation of PDK1, GSK3-β, PTEN and expression of Skp2 mRNA after ischemia/reperfusion injury in the mouse kidney

摘要: The aim of this study was to investigate the role 3-phosphoinositide-dependent protein kinase-1 (PDK1), glycogen synthase kinase-3β (GSK3-β) and phosphatase tensin homologue deleted on chromosome 10 (PTEN), which are components phosphoinositide 3-kinase (PI3K)/Akt pathway, expression S-phase kinase-associated 2 (Skp2) messenger RNA (mRNA) in renal ischemia/reperfusion. Three experimental groups, sham-operative mice, vehicle-delivered mice wortmannin-treated ischemia/reperfusion injury (IRI) were designed examine PDK1, GSK3-β PTEN phosphorylation status, as well Skp2 mRNA at 30 min, 90 min, 24 h 48 h reperfusion after ischemia treatment. Wortmannin or its vehicle given intraperitoneally 4 h before surgery. Expression examined by semiquantitative reverse-transcription PCR, PI3K/Akt pathway detected western blotting IRI kidney. Phosphorylation PDK1(Ser241), GSK3-β(Ser9) PTEN(Ser380) increased mouse kidney, PDK1 reduced wortmannin administration. mouse, could be inhibited wortmannin. Our primary suggests that signaling plays an important regulating repair following IRI. kidney may regulated pathway.