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Participation of platelet‐activating factor in the lipopolysaccharide‐induced liver injury in partially hepatectomized rats

Platelet‐activating factor (PAF) has been shown to be an important mediator in the pathogenesis of lipopolysaccharide (LPS)‐induced liver injury in regenerating rat livers. Both LPS and PAF activate nuclear factor‐kappa B (NF‐κB), a key transcription factor for tumor necrosis factor‐α (TNF‐α) and cytokine‐induced neutrophil chemoattractant (CINC). The aim of this study is to investigate how PAF participates in the LPS‐induced and NF‐κB–mediated regulation of TNF‐α and CINC in regenerating rat livers. LPS (1.5 mg/kg) was intravenously administered into 70% hepatectomized rats and sham‐operated rats 48 hours postoperatively. LPS administration caused a high mortality rate, scattered necrosis in the liver with infiltration of CINC‐positive neutrophils, and a continuous CINC messenger RNA up‐regulation and activation of NF‐κB in the liver only in hepatectomized rats. These phenomena were all effectively prevented by pretreatment and posttreatment with a PAF receptor antagonist, TCV‐309. Hepatectomized rats showed NF‐κB staining in hepatocytes, Kupffer cells, and neutrophils around necrosis 4 hours after the LPS injection, representing the activation of this factor in these cells. Based on these results, we propose that PAF contributes to continuous CINC up‐regulation and NF‐κB activationviaaccumulation and activation of neutrophils, and thereby is involved in LPS‐induced liver injury in regenerating rat livers.