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

Abstract

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.