title: [Effect of heme oxygenase on apoptosis and apoptosis genes in hepatic ischemia reperfusion injury in rats].
abstract: OBJECTIVE
  To use heme oxygenase (HO) inducer hemin and a HO inhibitor zinc protoporphyrin (ZnPP) to investigate the effect of HO on apoptosis and apoptosis genes in hepatic ischemia reperfusion (IR) injury in rats.
  
  
  METHODS
  Ninety-six Sprague-Dawley rats were randomly divided into four groups (24 rats in each): a sham-operation group, an ischemia-reperfusion (IR) group, a hemin-IR group and a ZnPP-IR group. Liver functions, liver histology and hepatocellular apoptosis rates were observed at 0, 1.5, 4 and 8 hours after reperfusion. Hepatocellular apoptosis was determined by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling; expressions of Bcl-2 and caspase-3 were determined by Western blot.
  
  
  RESULTS
  Compared with the sham-operation group, the levels of ALT and AST were increased in the IR group. In the IR group the histological changes found in the livers were swelling of hepatocytes, narrowing of hepatic sinusoids, inflammatory cell infiltration and necrosis of hepatocytes in some areas of the livers. In the IR group rate of hepatocellular apoptosis was increased at 0, 1.5, 4 and 8 hours after reperfusion; expression of Bcl-2 was decreased and the expression of caspase-3 was increased. In the hemin-IR group, the levels of ALT and AST were lower, the pathological changes were milder and the rate of hepatocellular apoptosis was lower at 0, 1.5, 4 and 8 hours in comparison to those of the IR group. The expression of Bcl-2 was higher and the expression of caspase-3 was lower in the hemin-IR group in comparison to those of the IR group. The results in the ZnPP-IR group were just the opposite to those of the hemin-IR group.
  
  
  CONCLUSIONS
  HO might play a protective role in hepatic IR injury in rats, and this effect may be related to the inhibition of hepatocellular apoptosis.
authors.affiliation: Department of Gastroenterology, Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, China.
authors.forename: Yang-Yang
authors.initials: YY
authors.lastname: Wang
authors.forename: Zhi-Jie
authors.initials: ZJ
authors.lastname: Feng
authors.forename: Yuan-Yuan
authors.initials: YY
authors.lastname: Yue
authors.forename: Mei
authors.initials: M
authors.lastname: Song
authors.forename: Wen-Jie
authors.initials: WJ
authors.lastname: Song
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D053148:Caspase 3 / Q000378:metabolism; D006419:Heme Oxygenase (Decyclizing) / Q000378:metabolism*; D022781:Hepatocytes / Q000378:metabolism / Q000473:pathology; D008107:Liver Diseases / Q000378:metabolism / Q000473:pathology*; D008297:Male; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D011524:Protoporphyrins / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000378:metabolism / Q000473:pathology*
chemical_list: D019253:Proto-Oncogene Proteins c-bcl-2; D011524:Protoporphyrins; C017803:zinc protoporphyrin; D006419:Heme Oxygenase (Decyclizing); D053148:Caspase 3