title: Contributions of heme oxygenase-1 in postconditioning-protected ischemia-reperfusion injury in rat liver transplantation.
abstract: BACKGROUND
  Heme oxygenase-1 (HO-1), an oxidative stress-response gene up-regulated by various physiological and exogenous stimuli, has cytoprotective activities. Ischemic postconditioning (Postcon) can protect an organ from ischemia-reperfusion (I/R) injury. In the present study, we investigated the potential contributions of HO-1 to Postcon-dependent protection against I/R injury in rat liver transplantation models.
  
  
  METHODS
  Adult male Sprague-Dawley rats were randomly divided into four groups: sham group with laparotomy for liver exposure; I/R group with 24-hour cold ischemia of the donor liver; Postcon group with the same treatment as the I/R group plus ischemic Postcon; and zinc protoporphyrin (ZnPP HO-1 inhibitor) + Postcon group treated the same as the Postcon cohort with donors pretreated using ZnPP 24 hours before the I/R injury. We measured liver tissue and peripheral blood samples collected at 6 hours after reperfusion and serum transaminase levels, histopathology, liver tissue malondialdehyde (MDA) content, superoxide dismutase (SOD) activity and HO-1 expression in the liver.
  
  
  RESULTS
  Postcon significantly diminished the elevation of serum transaminases levels after I/R injury when compared with I/R and ZnPP+Postcon groups. Postcon treated rats showed significantly lower MDA production and higher SOD activity. HO-1 was induced in rat livers exposed to Postcon; its levels were obviously overexpressed after 6 hours in Postcon rats. Inhibiting the expression of HO-1, negated the protective effects of Postcon.
  
  
  CONCLUSIONS
  Induction of HO-1 in the Postcon condition played a protective role against hepatic I/R injury and enhanced the early antioxidative activity. The protective effects of Postcon were significantly associated with greater intrahepatic HO-1 expression.
authors.affiliation: Organ Transplant Center, The First Affiliated Hospital of Kunming Medical College, Kunming, China. zzong@medmail.com.cn
authors.forename: Z
authors.initials: Z
authors.lastname: Zeng
authors.forename: H F
authors.initials: HF
authors.lastname: Huang
authors.forename: M Q
authors.initials: MQ
authors.lastname: Chen
authors.forename: F
authors.initials: F
authors.lastname: Song
authors.forename: Y J
authors.initials: YJ
authors.lastname: Zhang
mesh_terms: D000818:Animals; D001483:Base Sequence; D017931:DNA Primers; D006419:Heme Oxygenase (Decyclizing) / Q000235:genetics / Q000378:metabolism*; D007150:Immunohistochemistry; D008099:Liver / Q000201:enzymology / Q000378:metabolism / Q000503:physiopathology; D008111:Liver Function Tests; D016031:Liver Transplantation; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000201:enzymology*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013482:Superoxide Dismutase / Q000378:metabolism; D019172:Transplantation Conditioning
chemical_list: D017931:DNA Primers; D012333:RNA, Messenger; D008315:Malondialdehyde; D006419:Heme Oxygenase (Decyclizing); C491523:Hmox1 protein, rat; D013482:Superoxide Dismutase