Sepsis is a severe disease, with high mortality. Permanent organ damage caused by sepsis reduces the quality of life of surviving patients. The liver is an easily damaged organ in sepsis and sepsis‑associated liver injury foretells a poor prognosis. Unfortunately, there are no effective treatments or drugs to solve this problem. Therefore, strategies or novel drugs are urgently required to protect against liver dysfunction in sepsis. In the present study, lipopolysaccharide (LPS) was used to establish a model of liver injury in vitro. The data demonstrated that pretreatment of L02 human normal hepatocytes with paeonol (PAE) alleviated LPS‑induced cell injury and decreased the levels of alanine aminotransferase and aspartate transaminase, indicating a protective effect of PAE. Further experiments demonstrated that PAE increased LPS‑decreased L02 cell viability, the levels of superoxide dismutase and Bcl‑2 expression. PAE decreased LPS‑increased cell apoptosis, intracellular reactive oxygen species and the expression levels of Bax and cleaved‑caspase‑3. PAE decreased LPS‑promoted mitochondrial depolarization and nuclear translocation of NF‑κB. In conclusion, PAE alleviated LPS‑induced liver injury via alteration of mitochondrial function and NF‑κB translocation. Therefore, PAE has potential for the treatment of sepsis.
Keywords: liver injury; nuclear translocation of NF‑κB; paeonol; reactive oxygen species; sepsis.