title: Role of PI3-kinase/Akt signalling pathway in renal function and cell proliferation after renal ischaemia/reperfusion injury in mice.
abstract: BACKGROUND
  PI3K/Akt pathway has been shown to play a critical role in the regulation of mitogenic signalling, apoptosis, cell proliferation and survival in a variety of cells and tissues. The aim of the present study was to investigate the role of PI3K/Akt pathway in the renal ischaemia/reperfusion.
  
  
  METHODS
  Four experimental groups, sham-operative mice, vehicle-delivered and wortmannin-treated ischaemic/reperfusion injury mice, wortmannin-treated normal mice were designed to examined serum blood urea nitrogen level, renal injury, proliferating cell nuclear antigen protein and Akt phosphorylation status at 30 min, 90 min, 24 h, 48 h of reperfusion after ischaemic treatment. Wortmannin or its vehicle was given intraperitoneally at 4 h before surgery. Blood urea nitrogen was measured, and immunohistochemistry and western blotting were used to detect the components of PI3K/Akt pathway in the ischaemic/reperfusion injury kidney.
  
  
  RESULTS
  PI3-kinase inhibitor wortmannin imposes a deleterious effect on serum blood urea nitrogen level, renal function after renal ischaemia/reperfusion injury in mice. The renal cell proliferation increased after ischaemia/reperfusion injury in mouse, which could be inhibited by wortmannin. Phosphorylation of Akt was increased after ischaemia/reperfusion in the mouse kidney, and reduced by wortmannin administration.
  
  
  CONCLUSIONS
  This primary study suggests that PI3-kinase/Akt signalling pathway play an important role in the regulation of the renal repair after ischaemia/reperfusion injury.
authors.affiliation: Department of Urology, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.
authors.forename: Liping
authors.initials: L
authors.lastname: Xie
authors.forename: Xiangyi
authors.initials: X
authors.lastname: Zheng
authors.forename: Jie
authors.initials: J
authors.lastname: Qin
authors.forename: Zhaodian
authors.initials: Z
authors.lastname: Chen
authors.forename: Yongfeng
authors.initials: Y
authors.lastname: Jin
authors.forename: Wei
authors.initials: W
authors.lastname: Ding
mesh_terms: D000818:Animals; D001806:Blood Urea Nitrogen; D049109:Cell Proliferation; D048430:Cell Shape; D007668:Kidney / Q000473:pathology / Q000502:physiology*; D007674:Kidney Diseases / Q000097:blood / Q000201:enzymology* / Q000473:pathology*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism*; D010766:Phosphorylation; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism*; D015427:Reperfusion Injury / Q000097:blood / Q000201:enzymology* / Q000473:pathology*; D015398:Signal Transduction
chemical_list: D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt