【Abstract】：ObjectiveTo investigate the effect of recombinant human granulocyte colony-stimulating factor (rhG-CSF) on acute liver failure (ALF) induced by D-galactosamine (D-GalN) in rats. MethodsA total of 105 male Sprague-Dawley rats were randomly divided into healthy control group, liver failure model group, and rhG-CSF group, with 35 rats in each group. A rat model of ALF was established by intraperitoneal injection of D-GalN (1400 mg/kg). Alanine aminotransferase (ALT) level in the liver, total bilirubin (TBil), peripheral blood leukocyte count, and liver pathological changes were observed at 12, 24, 48, 72, and 120 hours after modeling, and survival rate was observed at 120 hours after modeling. A one-way analysis of variance was used for comparison of continuous data between multiple groups, and the LST-t test was used for further comparison between two groups. ResultsCompared with the liver failure model group, the rhG-CSF group had a significantly higher degree of hepatocyte degeneration and necrosis at all time points except 120 hours after modeling, and compared with the liver failure model group at 120 hours after modeling, the rhG-CSF group had better recovery of lobular structure on HE staining. Compared with the liver failure model group, the rhG-CSF group had a tendency of increase in the percentage of cells with positive tumor necrosis factor-α at the five time points after modeling. Compared with the liver failure model group, the rhG-CSF group had significantly higher levels of ALT and TBil at all five time points. Both groups had a significant change in ALT level at 24 hours after modeling (P＜0.05), as well as a significant change in TBil at 24, 48, and 120 hours after modeling (P＜0.05). The rhG-CSF group had a significantly higher peripheral blood leukocyte count than the liver failure model group at all five time points (all P＜005). There was no significant difference in survival rate at 120 hours after modeling between the two groups (P＞0.05). ConclusionApplication of rhG-CSF during the stage of acute inflammatory reaction of ALF may aggravate liver inflammatory response.
【Key words】：liver failure, acute； granulocyte colony stimulating factor； D-galactosamine； tumor necrosis factor-alpha； rats, Sprague-Dawley； disease models, animal