The aerial part of Taraxacum coreanum extract has an anti-inflammatory effect on peritoneal macrophages in vitro and increases survival in a mouse model of septic shock

Abstract

Ethnopharmacological relevance: Taraxacum coreanum Nakaiis a dandelion native to Korea and is widely consumed as an edible and medicinal herb. The aerial part of Taraxacum coreanum (TC) has been used therapeutically as a diuretic and anti-inflammatory agent, but its mechanism of action has not yet been evaluated.

Aim of the study: To investigate the anti-inflammatory potential of a Taraxacum coreanum chloroform fraction(TCC) and its mechanisms of action in vitro and in vivo.

Materials and methods: Isolated mouse peritoneal macrophages were stimulated in vitro with interferon-γ (IFN-γ) and lipopolysaccharide (LPS) in the presence or absence of TCC. The anti-inflammatory effects of TCC were assessed by measuring nitric oxide (NO) and prostaglandin E2 (PGE2) production, as well as expression of inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), IκBα, phospho-IKK, mitogen-activated protein kinases (MAPKs), and signal transducer and activator of transcription (STAT1). The effects of TCC were tested in vivo by measuring cytokine production and survival in a mouse model of lethal septic shock. And the standard compounds of Taraxacum coreanum were analyzed by HPLC using a C18 column.

Results: Treatment of primary macrophages with TCC in vitro significantly inhibited all of the inflammatory parameters measured, including LPS-induced NO and PGE2 production, iNOS and COX-2 expression, IκBα degradation, IKK phosphorylation, and MAPK and STAT1 activation. In a mouse model of LPS-induced septic shock, TCC inhibited the production of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6, and increased survival by 83%.Standard compounds (gallic acid, syringic acid) of Taraxacum coreanum were qualified by HPLC analysis.

Conclusions: TCC possesses potent anti-inflammatory activity in vitro and in vivo, which occurs at least partly through inhibition of proinflammatory signaling and mediator release. These results strongly support the therapeutic potential of TCC as an anti-inflammatory agent in vivo.