Flower extract of Panax notoginseng attenuates lipopolysaccharide-induced inflammatory response via blocking of NF-kappaB signaling pathway in murine macrophages

Abstract

Aim of the study: The root of Panax notoginseng (PN) is commonly used to treat chronic liver disease with its therapeutic abilities to stop haemorrhage in the circulation, while the PN flower (PN-F) is largely unknown in the biological activities on inflammation and mechanisms of its actions. In this study, the pharmacologic effects of PN-F methanol extract on inflammation were investigated to address potential therapeutic or toxic effects in LPS-stimulated mouse macrophage cells, RAW264.7 cells.

Materials and methods: Production of NO, PGE2 and pro-inflammatory cytokines (TNF-alpha and IL-1beta) in supernatant, the expression of iNOS, COX-2 and cytokines, the phosphorylation of MAPK molecules (ERK1/2, JNK and p38 MAPK), and the activation of NF-kappaB in PN-F extract were assayed in LPS-stimulated RAW264.7 cells.

Results: PN-F extract significantly inhibited the productions of NO, PGE2, TNF-alpha and IL-1beta on the LPS-stimulated RAW264.7 cells. In addition, PN-F extract suppressed the mRNA and protein expressions of iNOS, COX-2, TNF-alpha and IL-1beta in LPS-stimulated RAW264.7 cells. The molecular mechanism of PN-F extract-mediated attenuation in RAW264.7 cells has close a relationship to suppressing the phosphorylation of MAPK molecules such as ERK1/2, JNK and p38 MAPK, and the translocation of NF-kappaB p65 subunit into nuclear.

Conclusion: These results indicate that PN-F extract inhibits LPS-induced inflammatory response via the blocking of NF-kappaB signaling pathway in macrophages, and demonstrated that PN-F extract possesses anti-inflammatory properties in vitro.