Effect of propofol on liver injury in mice with acute liver failure / 中华麻醉学杂志

ABSTRACT

Objective To evaluate the effect of propofol on liver injury in mice with acute liver failure (ALF).Methods Eighty adult male ICR mice,aged 1 months,weighing 20-25 g,were randomly divided into 3 groups (n =20 each) using a random number tablecontrol group (group Ⅰ),ALF group (group Ⅱ),and ALF + propofol group (group Ⅲ).ALF model was established with intra-peritoneal D-galactosamine (D-GaIN) and lipopolysaccharide (LPS).Propofol 5 mg/kg was injected via the tail vein every 1 h within 6 h after injection of DGaIN and LPS in group Ⅲ,while the equal volume of normal saline was given instead in the other groups.Venous blood samples were taken from the tail vein at 1,3 and 6 h after injection of D-GaIN and LPS (T1-3) to detect the activities of serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) and serum tumor necrosis factor-alpha (TNF-α),interleukin-1β (IL-1β) and IL-10 concentrations (by ILISA).The survival within 12 h after injection of D-GaIN and LPS was observed and the survival rates were calculated.The mice were sacrificed and livers were removed for microscopic examination of pathologic changes.Results Compared with group Ⅰ,the activities of AST and ALT were significantly increased at each time point in Ⅱ and Ⅲ groups and the serum TNF-α concentrations at T1,2 and IL-1β and IL-10 concentrations at each time point were significantly increased in group Ⅱ,and the serum TNF-α concentrations at T1,and IL-1β and IL-10 concentrations at T2,3 were significantly increased in group Ⅲ (P ＜ 0.05).Compared with group Ⅱ,the activities of AST and ALT at each time point,serum TNF-α concentrations at T1,2 and IL-1β and IL-10 concentrations at T2,3 were significantly decreased and the survival rate within 12 h after injection of D-GaIN and LPS was increased in group Ⅲll (P ＜ 0.05).The pathologic changes of liver tissues were gradually attenuated in Ⅱ and Ⅲ groups.Conclusion Propofol can reduce the liver injury in mice with ALF through inhibiting inflammatory responses.