Objective To establish mouse acute liver injury model and lethal model induced by lipopolysaccharide (LPS) injection alone.Methods Mice were injected intraperitoneally ( i.p.) with different concentrations of LPS (0,10,30,50,80 mg/kg).The physiological statuses of mice were observed.The liver tissue of mice was stained by Hematoxylin and Eosin (HE) to examine the injury of the liver.The levels of tumor necrosis factor (TNF)-α in mouse serum were detected by enzyme linked immunosorbent assay (ELISA).The expression and nuclear translocation of nuclear factor (NF)-κB p65 in mouse liver tissue were measured by immunohistochemistry staining.Results No death and liver injury were found in control group mice.No increased NF-κB p65 protein expression and nuclear translocation in liver tissue and increased serum TNF-α levels were detected in control group mice.No deaths of mice were found in group with intraperitoneal injection of LPS at a concentration of 30 mg/kg.As compared with the control group,liver injury,increased NF-κB p65 protein expression and nuclear translocation in liver tissue and increased serum TNF-α levels were detected in this group ( P ＜ 0.01 ).Mice with intraperitoneal injection of LPS at a concentration of LPS 50mg/kg survived no more than 120 h.As compared with the control group,liver injury,significantly increased NF-κB p65 protein expression and nuclear translocation in liver tissue and significantly increased serum TNF-α levels were detected in this group (P ＜0.01 ).Conclusion Our research successfully establishes mice liver injury model and lethal model induced by LPS intraperitoneal injection alone,which provides stable research platform for further medical treatment.