Chikusetsusaponin IVa (CHS-IVa), a saponin from herb Panacis japonicas, possesses extensive biological activities. However, the roles and underlying mechanisms of CHS-IVa on inflammation have not been fully clarified in the setting of murine macrophages. In this study, we found that CHS-IVa effectively reduced the expression of inflammatory mediators, including interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), interleukin-10 (IL-10), interleukin-1β (IL-1β), cyclooxygenase (COX-2), inducible nitric oxide synthase (iNOS) in lipopolysaccharide (LPS)-stimulated murine macrophage-like RAW264.7 cells. Meanwhile, CHS-IVa could also evidently bate the contents of nitric oxide (NO) and prostaglandin E2 (PGE2) in cell culture supernatants. Furthermore, the anti-inflammatory activity of CHS-IVa may be via diminishing the phosphorylation of extracellular regulated protein kinases (ERK), p38, and c-Jun N-terminal kinase (JNK). Collectively, these findings will help to understand of the anti-inflammatory effects and mechanisms of P. japonicas deeply, and suggest a validated therapeutic use as an anti-inflammatory medication.
Keywords: MAPK; chikusetsusaponin IVa; inflammation; murine macrophage-like cells.
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