title: Roles of MAPKAPK-2 and HSP27 in the reduction of renal ischemia-reperfusion injury by ischemic postconditioning in rats.
abstract: OBJECTIVE
  Ischemic postconditioning is a procedure during which intermittent reperfusions are performed in the early phase of reperfusion to protect organs from ischemia/reperfusion injury. And in this study, we mainly investigated the injury-alleviative role of mitogen-activated protein kinase-activating protein kinase-2 (MAPKAPK-2) and heat shock protein 27 (HSP27) in renal ischemic reperfusion injury during the procedure of ischemic postconditioning.
  
  
  METHODS
  Sprague-Dawley rats were randomly divided into four groups. The injury models were prepared by clipping the left renal pedicle of rats after ligating the right renal pedicle for 60 min. In the ischemic postconditioning group, sequential reperfusions were done for 10 s and another ischemia for 10 s for six cycles after kidney ischemia for 60 min. In addition, the specific inhibitor SB203580 was injected through caudal vein before ischemia. Serum creatinine, blood urea nitrogen and the expression of HSP27 and MAPKAPK-2 were detected 1, 3, 6 and 24 h later after reperfusion. Furthermore, phosphorylation of HSP27 and MAPKAPK-2 protein contents, histological changes and apoptosis were compared 24 h later after reperfusion.
  
  
  RESULTS
  Our data showed that ischemic postconditioning attenuated the renal dysfunction and cell apoptosis induced by I/R and increased phosphorylation of MAPKAPK-2 and HSP27. The results indicated that ischemic postconditioning decreased apoptosis and improved renal function.
  
  
  CONCLUSIONS
  Taken together, it is suggested that the renal protective effect may be related to the levels of HSP27 and MAPKAPK-2 activation.
authors.affiliation: Department of Pharmacology, School of Pharmacy, Xuzhou Medical College, 209 Tongshan Road, Xuzhou, 221004, Jiangsu Province, China, xaz2008190@sina.com.
authors.forename: Anzhou
authors.initials: A
authors.lastname: Xia
authors.forename: Yong
authors.initials: Y
authors.lastname: Li
authors.forename: Na
authors.initials: N
authors.lastname: Li
authors.forename: Zhi
authors.initials: Z
authors.lastname: Xue
authors.forename: Jieyun
authors.initials: J
authors.lastname: Xia
authors.forename: Tiantian
authors.initials: T
authors.lastname: Wei
authors.forename: Jing
authors.initials: J
authors.lastname: Cao
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology; D001806:Blood Urea Nitrogen; D003404:Creatinine / Q000097:blood; D055551:HSP27 Heat-Shock Proteins / Q000502:physiology*; D007150:Immunohistochemistry; D047908:Intracellular Signaling Peptides and Proteins / Q000502:physiology*; D057775:Ischemic Postconditioning; D007668:Kidney / Q000098:blood supply* / Q000473:pathology; D008297:Male; D017346:Protein Serine-Threonine Kinases / Q000502:physiology*; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000503:physiopathology* / Q000517:prevention & control*; D015854:Up-Regulation / Q000502:physiology; D000099190:MAP-Kinase-Activated Kinase 2
chemical_list: D003404:Creatinine; D055551:HSP27 Heat-Shock Proteins; D047908:Intracellular Signaling Peptides and Proteins; D017346:Protein Serine-Threonine Kinases; D000099190:MAP-Kinase-Activated Kinase 2