Suppression of tumor necrosis factor-α production and neutrophil infiltration during ischemia–reperfusion injury of the liver after heat shock preconditioning

Background/Aims: 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-α (TNF-α) production and neutrophil infiltration. Methods: Rats were exposed to heat shock pretreatment at 42°C in the heat shock group (group HS) and at 37°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-α, cytokine-induced neutrophil chemoattractant (CINC) and alanine aminotransferase (ALT) were measured. Liver tissues were checked for the presence of TNF-α mRNA. Histological staining for CINC and polymorphonuclear leukocyte (PMN) was also evaluated. Results: In group HS, plasma TNF-α levels were significantly more suppressed than in group C (P<0.0001). Expressions of TNF-α 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-α and CINC in the liver during reperfusion and consequently reduced neutrophil infiltration.