Heliangin inhibited lipopolysaccharide-induced inflammation through signaling NF-κB pathway on LPS-induced RAW 264.7 cells.

Abstract

The heliangin is a natural agent mainly isolated from Helianthus tuberosus L. (Asteraceae). In order to investigate the anti-inflammatory effect of heliangin, several typical models in vivo and in vitro were performed. The RAW264.7 mouse macrophages cells were employed in vitro and dexamethasone were conducted as positive. The cytotoxicity results of heliangin on RAW 264.7 cells provided the safety in vitro for further study. The mRNA of TNF-α, IL-6, iNOS and COX-2 were degraded under heliangin exposure in LPS-stimulated RAW 264.7 cells. The protein expression of iNOS, COX-2 were decreased via heliangin exposure in a dose-dependent manner. Heliangin inhibited TNF-α, NO, IL-6 and PGE2 expression levels in macrophage cells lysate. The immunocytochemistry assay showed the fluorescence image of heliangin treatment intercepted the p65 translocation process from outside to inside of nuclei triggered by LPS. Moreover, we founded that MAPK and NF-κB signaling pathway play important roles in heliangin's activity on RAW264.7 cells. Secondly, the acute toxic study results of heliangin manifested the safety in vivo. Heliangin exerted anti-inflammation effect in a xylene-induced ear swelling in BALB/C mice and carrageenan-induced paw edema model in SD rats. The cytokines levels (TNF-α, IL-6 and PGE2) were decreased. The paw tissue immunochemistry assay demonstrated the IL-6 protein level changes in carrageenan-induced paw edema model under heliangin administration.