Recombinant C-terminal heparin-binding domain of fibronectin polypeptide protects against liver damage, reduces serum inflammatory cytokines, and decreases mortality in acute liver failure.

This study aimed to evaluate the effect of recombinant C-terminal heparin-binding domain of fibronectin (FNCHBD) polypeptide on live-damage protection, inflammation, and mortality in acute liver failure (ALF) mice. 25 mice were randomly divided into five groups: normal controls, lipopolysaccharide (LPS)/D-galactosamine (GalN), 5 mg/kg FNCHBD, 10 mg/kg FNCHBD and 20 mg/kg FNCHBD groups. Blood samples were obtained at 9 h after treatment for measurement of liver indexes and inflammatory cytokine levels, and livers were acquired for H&E and TUNEL staining assays. 90 mice (18 mice in each group) were randomly divided into five groups for mortality assessment after LPS/GalN administration at 48 h. Compared to LPS/GalN group, levels of blood liver indexes including AST, ALT and TBIL were decreased in FNCHBD polypeptide-treated groups. H&E staining disclosed FNCHBD polypeptide protected cell morphology and histomorphology, and necrosis rates in FNCHBD polypeptide-treated groups were lower compared to LPS/GalN group. TUNEL staining assay revealed cell apoptosis was inhibited in FNCHBD polypeptide-treated groups compared to LPS/GalN group. Serum inflammatory cytokines including TNF-α, IL-1β, and IL-6 were reduced in FNCHBD polypeptide-treated groups compared to LPS/GalN group. As to mortality rate, it was only decreased in 10 mg/kg FNCHBD and 20 mg/kg FNCHBD groups but not in 5 mg/kg FNCHBD compared to LPS/GaIN group. In addition, most effects of FNCHBD presented in a dose-dependent manner. FNCHBD polypeptide protects against liver damage, inhibits elevation of serum inflammatory cytokines, and decreases mortality in ALF.