title: Suppression of tumor necrosis factor-alpha production and neutrophil infiltration during ischemia-reperfusion injury of the liver after heat shock preconditioning.
abstract: OBJECTIVE
  Heat shock preconditioning provides the liver with ischemic tolerance. In this study we examined the effects of heat shock preconditioning on hepatic nonparenchymal cells in light of tumor necrosis factor-alpha (TNF-alpha) production and neutrophil infiltration.
  
  
  METHODS
  Rats were exposed to heat shock pretreatment at 42 degrees C in the heat shock group (group HS) and at 37 degrees C in the control group (group C). After a 48-h recovery, the left hepatic lobes were given a 90-min ischemia and reperfused. Plasma concentrations of TNF-alpha, cytokine-induced neutrophil chemoattractant (CINC) and alanine aminotransferase (ALT) were measured. Liver tissues were checked for the presence of TNF-alpha mRNA. Histological staining for CINC and polymorphonuclear leukocyte (PMN) was also evaluated.
  
  
  RESULTS
  In group HS, plasma TNF-alpha levels were significantly more suppressed than in group C (P<0.0001). Expressions of TNF-alpha mRNA in the liver was suppressed in group HS. Production of CINC 2 h after reperfusion was reduced in group HS (P<0.05). PMN infiltration was significantly reduced in group HS (P<0.01). In group HS, liver histology revealed less cellular damage and the plasma level of ALT was significantly reduced (P<0.0001).
  
  
  CONCLUSIONS
  Heat shock preconditioning suppressed the production of TNF-alpha and CINC in the liver during reperfusion and consequently reduced neutrophil infiltration.
authors.affiliation: Department of Gastroenterological Surgery, Kyoto University Graduate School of Medicine, 54 Kawahara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Yonezawa
authors.forename: Y
authors.initials: Y
authors.lastname: Yamamoto
authors.forename: H
authors.initials: H
authors.lastname: Yamamoto
authors.forename: Y
authors.initials: Y
authors.lastname: Ishikawa
authors.forename: H
authors.initials: H
authors.lastname: Uchinami
authors.forename: K
authors.initials: K
authors.lastname: Taura
authors.forename: A
authors.initials: A
authors.lastname: Nakajima
authors.forename: Y
authors.initials: Y
authors.lastname: Yamaoka
mesh_terms: D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D019743:Chemokines, CXC; D002630:Chemotactic Factors / Q000097:blood; D004797:Enzyme-Linked Immunosorbent Assay; D005786:Gene Expression Regulation / Q000502:physiology*; D006133:Growth Substances / Q000097:blood; D006358:Hot Temperature; D036341:Intercellular Signaling Peptides and Proteins; D019194:Ischemic Preconditioning; D008102:Liver Circulation / Q000502:physiology*; D008297:Male; D009504:Neutrophils / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D012016:Reference Values; D015427:Reperfusion Injury / Q000235:genetics / Q000503:physiopathology*; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics*
chemical_list: D019743:Chemokines, CXC; D002630:Chemotactic Factors; C513294:Cxcl3 protein, rat; D006133:Growth Substances; D036341:Intercellular Signaling Peptides and Proteins; D014409:Tumor Necrosis Factor-alpha; D000410:Alanine Transaminase