Araliasaponin II isolated from leaves of Acanthopanax henryi (Oliv.) Harms inhibits inflammation by modulating the expression of inflammatory markers in murine macrophages.

Araliasaponin II (AS II) is a bioactive compound isolated from Acanthopanax henryi (Oliv.) Harms, a plant widely used in traditional oriental medicine. The present study investigated the anti‑inflammatory effects of AS II using murine macrophages. The effects of AS II on inflammatory mediator and cytokine production in lipopolysaccharide (LPS)‑stimulated RAW 264.7 cells was evaluated. Nitric oxide (NO) and cytokine production were determined using the Griess reagent and an ELISA kit. The expression levels of cytokines, inducible NO synthase (iNOS) and cyclooxygenase‑2 (COX‑2) mRNA were examined by reverse transcription‑quantitative polymerase chain reaction. The expression levels of iNOS, COX‑2 and toll‑like receptor (TLR)‑4 protein were examined by western blotting. Translocation of nuclear factor‑κB (NF‑κB) and TLR‑4 expression were visualized by immunofluorescence staining. AS II markedly inhibited the production of NO and prostaglandin E2, and reduced iNOS and COX‑2 expression at the transcriptional and translational levels. AS II downregulated the expression of interleukin‑6 and tumor necrosis factor‑α at the protein and mRNA levels. Furthermore, pre‑treatment with AS II significantly suppressed the TLR‑4‑NF‑κB signaling pathway; this effect may be cause by AS II competing with LPS for binding to TLR‑4 and subsequently inhibiting translocation of the NF‑κB/p65 protein to the nucleus. The results suggested that the anti‑inflammatory properties of AS II may result from inhibiting pro‑inflammatory mediators by suppressing the initiation of the inflammatory response and inhibiting TLR-4-NF-κB signaling pathways.