Abstract: To explore the effect of lowdose lipopolysaccharide (LPS) on acute liver injury induced by highdose lipopolysaccharide in mice. MethodsThe mouse model of acute liver injury was reproduced by intraperitoneal administration of LPS. GSH in the livers of mice was depleted by administering buthionine sulphoximine (BSO). Aspartate transaminase (AST) and alanine transaminase (ALT) in the plasma were measured by an automated biochemistry analyzer. The mRNA levels of cystathione (synthase (CBS) and γglutamylcysteine synthetase (GCS) were determined by RTPCR. Results① Pretreatment with lowdose LPS attenuated acute liver injury induced by highdose LPS in mice. ② Lowdose LPS treatment elicited hepatic glutathione (GSH) levels in mice. The levels of GSH in the group pretreated with lowdose LPS were higher than those in the group treated with highdose LPS. ③ Plasma levels of ALT and AST in the group pretreated with lowdose LPS were similar to those in the group treated with highdose LPS. ④ Lowdose LPS pretreatment resulted in an increase in CBS activity as well as GSC mRNA levels. ConclusionLowdose LPS attenuates acute liver injury induced by highdose LPS in mice by promoting hepatic GSH levels though upregulating activity or expression of GSH biosynthesisrelative genes.

Key words: Lipopolysaccharide, Liver injury, Glutathione, Cystathionine betasynthase, γGlutamylcysteine synthetase, mice