Saikosaponin‑d alleviates carbon‑tetrachloride induced acute hepatocellular injury by inhibiting oxidative stress and NLRP3 inflammasome activation in the HL‑7702 cell line.

Saikosaponin‑d (SSd) the primary active component of triterpene saponin derived from Bupleurum falcatum L., possesses anti‑inflammatory and antioxidant properties. The present study aimed to examine the potential therapeutic effects of SSd on carbon tetrachloride (CCl4)‑induced acute hepatocellular injury in the HL‑7702 cell line and its underlying mechanisms. HL‑7702 cells were treated with SSd at different doses (0.5, 1 or 2 µmol/l). Cell viability was determined using an MTT assay. Injury was assessed by the levels of serum alanine aminotransferase (ALT) and aspartate transaminase (AST). Oxidative stress was assessed using malondialdehyde (MDA) content and total‑superoxide dismutase (T‑SOD) activity. The expression of nucleotide‑binding domain, leucine‑rich‑containing family, pyrin domain‑containing‑3 (NLRP3), apoptosis‑associated speck‑like protein (ASC), caspase‑1 and high mobility group protein B1 (HMGB1) was assessed by reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) and western blot analysis. Interleukin (IL)‑1β and IL‑18 were determined by RT‑qPCR and ELISA. SSd attenuated the inhibition of cell viability and the high AST and ALT levels induced by CCl4 in HL‑7702 cells. Oxidative stress was induced in HL‑7702 cells by CCl4, as demonstrated by the increase of MDA and the decrease of T‑SOD activity. These changes were reversed by SSd. SSd significantly downregulated the mRNA and protein expression of NLRP3, ASC, caspase‑1, IL‑1β, IL‑18 and HMGB1 induced by CCl4. In conclusion SSd alleviated CCl4‑induced acute hepatocellular injury, possibly by inhibiting oxidative stress and NLRP3 inflammasome activation in the HL‑7702 cell line.