Saikosaponin a ameliorates lipopolysaccharide and d‑galactosamine-induced liver injury via activating LXRα.

Saikosaponin a (SSa), one of the major active components of Bupleurum falcatum , has antioxidant and anti-inflammatory pharmacological properties. However, the effects of SSa on liver injury have not been reported. In the present study, we evaluated the protective effects and mechanisms of SSa on lipopolysaccharide (LPS)/ d ‑galactosamine (D-GalN)-induced liver injury. The mice were pretreated with SSa 1 h before LPS/D-GalN treatment. The liver MPO, MDA, and the serum AST and ALT levels were tested by specific determination kits. The pro-inflammatory cytokines TNF-α and IL-1β were tested by ELISA kits. The expression of NF-κB signaling pathway and LXRα were tested by western blot analysis. The results showed that SSa significantly reduced the levels of liver MPO, MDA, and serum AST, ALT levels induced by LPS/D-GalN. SSa also dose-dependently inhibited LPS/D-GalN-induced pro-inflammatory cytokines TNF-α and IL-1β production. Furthermore, we found that SSa inhibited NF-κB signaling pathway activation induced by LPS/D-GalN. In addition, SSa dose-dependently increased the expression of LXRα. In conclusion, the results demonstrated that SSa had protective effect on liver injury and the anti-inflammatory mechanisms of SSa on LPS/D-GalN-induced liver injury may be due to its ability to increase LXRα expression. SSa might be a potential treatment for liver injury. • SSa significantly reduced the levels of liver MPO, MDA, and serum AST, ALT levels induced by LPS/D-GalN. • SSa also dose-dependently inhibited LPS/D-GalN-induced TNF-α, and IL-1β production. • SSa inhibited NF-κB signaling pathway activation induced by LPS/D-GalN. • SSa dose-dependently increased the expression of LXRα. [ABSTRACT FROM AUTHOR]