ABSTRACT
Objective To investigate the liver repair effects of Pim-3 gene in rat with fulminant hepatic failure (FHF). Methods Thirty-two rats were divided into four groups (eight for each group). Three groups of rats were pretreated with Ringer's solution, vector plasmid or Pim-3 gene recombinant plasmid respectively and, one day later, received intraperitoneal injections with lipopolysacchride (LPS) and D-galactosamine (D-GalN). The fourth group served as normal control.Eight hours after the LPS/D-GalN injection, the liver tissues and blood samples were collected. The contents of serum transaminase was tested by automatic blood biochemistry meter. The morphological changes were observed by light microscopy using hematoxylin and eosin (HE) staining. Tumor necrosis factor (TNF)-α and interleukin (IL)-1β gene expression was detected by reverse transcriptionpolymerase chain reaction(RT-PCR). The serum levels of TNF-α and IL-1β were measured by enzyme linked immunosorbent assay (ELISA), and cell apoptosis by TdT-mediated dUTP nick end labeling (TUNEL) assay. Comparisons between groups were done by analysis of variance. ResultsThe over expressions of Pim-3 gene and reporter gene, green fluorescent protein (GFP) were induced by injection with recombinant plasmid solution.In comparison with the rats retreated with Ringer' s solution or vector plasmid, those pretreated with recombinant plasmid had a lower mortality and lower serum transaminase levels. The injection of recombinant plasmid significantly reduced hemorrhage, necrosis and inflammatory infiltration in the liver. Liver apoptotic index (AI) was dramatically lower in rats treated with recombinant vectors compared to the rats treated with Ringer's solution or vector plasmids [(10. 2±6.9)％ vs (83. 1±12.6) ％ and (79.9±13.4) ％ respectively, P＜0. 01]. In addition, the expression of exogenous Pim-3 gene remarkable inhibited the transcriptions and expressions of TNF-α and IL-1β. ConclusionsPim-3 gene can protect rats from LPS/D-GalN-induced FHF possibly by inhibiting expressions and secretions of inflammatory cytokines, such as TNF-α and IL-13, in liver tissues.