Hostaflavone A from Hosta plantaginea (Lam.) Asch. blocked NF-κB/iNOS/COX-2/MAPKs/Akt signaling pathways in LPS-induced RAW 264.7 macrophages.

ABSTRACT

ETHNOPHARMACOLOGICAL RELEVANCE Hostaflavone A (HA) is a new flavonoid component isolated from the flower of Hosta plantaginea (Lam.) Asch., which is commonly used as a folk herbal to treat inflammatory diseases in China. Nevertheless, the anti-inflammatory effect of HA remains unknown. AIM OF THE STUDY This work aimed to evaluate the HA with anti-inflammatory activity and mechanism in RAW 264.7 macrophages activated by lipopolysaccharide (LPS). MATERIALS AND METHODS: Anti-inflammatory effect of HA was evaluated by measuring of cell viability, nitric oxide (NO), prostaglandin E2 (PGE2), tumor necrosis factor α (TNF-α), interleukin 1ß (IL-1ß) and IL-6 levels in RAW 264.7 cells. In parallel, the HA action mechanism of nuclear factor kappa B (NF-κB) p65, inhibitor of NF-κB (IκB), inducible nitric oxide synthase (iNOS), cyclooxygenase 2 (COX-2), c-Jun N-terminal kinases (JNK), extracellular signal-regulated kinase (Erk), p38, and protein kinase B (Akt) were detected by Western blot analysis. RESULTS: HA has no cytotoxicity at concentrations as high as 40 µM. Besides, HA concentration-dependently clearly suppressed the overproduction of NO, PGE2, TNF-α, IL-1ß and IL-6 in RAW 264.7 cells induced by LPS. In addition, HA remarkably reduced the upregulation of phosphorylated NF-κB p65, phosphorylated IκB, phosphorylated JNK, phosphorylated Erk and phosphorylated p38, together with iNOS and COX-2 protein expressions in a concentration-dependent manner. CONCLUSION: HA blocked the LPS activated inflammation via suppressing NF-κB, iNOS, COX-2, mitogen-activated protein kinases (MAPKs) and Akt pathways in RAW 264.7 cells, and might be a new anti-inflammatory agent.