Anti-inflammatory effect of Sosihotang via inhibition of nuclear factor-κB and mitogen-activated protein kinases signaling pathways in lipopolysaccharide-stimulated RAW 264.7 macrophage cells

Sosihotang (SO) is an herbal medication, which has been widely used to treat fever, chill and vomiting due to common cold in east-Asian countries. In this study, to provide insight into the effects of SO on inflammation, we investigated its effect on pro-inflammatory mediator production in RAW 264.7 cells and mouse peritoneal macrophages using lipopolysaccharide (LPS) stimulation. SO significantly inhibited the production of nitric oxide (NO), tumor necrosis factor (TNF)-α and interleukin (IL)-6 as well as gene expression of inducible nitric oxide synthase (iNOS), its synthesizing enzyme. In addition, SO inhibited nuclear factor (NF)-κB activation and suppressed extracellular signal-regulated kinase (ERK), p38 and c- Jun NH2-terminal kinase (JNK) mitogen-activated protein kinases (MAPKs) phosphorylation. Furthermore, we found SO suppresses the production of NO and IL-6 in LPS-stimulated peritoneal macrophage cells. High performance liquid chromatography (HPLC) analysis showed SO contains many active anti-inflammatory constituents such as liquiritigenin, baicalin, baicalein, glycyrrhizin and wogonin. We first elucidated the inhibitory mechanism of SO on inflammation induced by LPS in macrophage cells. Our results suggest SO has potential to be developed as a therapeutic agent for various inflammatory diseases.