The anti-inflammatory effect of Lithospermum Erythrorhizon on lipopolysaccharide - induced inflammatory response in RAW 264.7 cells

Abstract

Objective : Lithospermum Erythrorhizon (LE) has been used as an anti-bacterial and anti-inflammatory agent. However, it is unclear that LE aqueous extract could show the anti-inflammatory effects in RAW 264.7cells. The purpose of this study was to investigate the anti-inflammatory effect of aqueous extract from LE on lipopolysaccharide (LPS) - induced inflammatory response. Methods : To measure out the cytotoxicity of LE, we performed the MTT assay. To evaluate the anti-inflammatory effects of LE, we examined the inflammatory mediators such as nitric oxide (NO), prostaglandin E2 (<TEX>$PGE_2$</TEX>) and pro-inflammatory cytokines (tumor necrosis factor (TNF)-<TEX>${\alpha}$</TEX>, interleukin, (IL)-<TEX>$1{\beta}$</TEX> and (IL)-6) on RAW 264.7 cells. We also examined molecular mechanisms such as mitogen-activated protein kinases (MAPKs) and nuclear factor-B (NF-<TEX>${\kappa}B$</TEX>) activation by western blot. Results : Aqueous Extract from LE itself did not have any cytotoxic effect in RAW 264.7 cells. Aqueous extract from LE inhibited LPS-induced productions of inflammatory mediators such as NO, <TEX>$PGE_2$</TEX>, and pro-inflammatory cytokines including TNF-<TEX>${\alpha}$</TEX>, IL-<TEX>$1{\beta}$</TEX> and IL-6 in RAW 264.7cells. In addition, LE inhibited the phosphorylation of p38 kinases (p38), c-Jun <TEX>$NH_2$</TEX>-terminal kinase (JNK), and NF-<TEX>${\kappa}B$</TEX> activation in RAW 264.7 cells. Conclusion : LE down-regulated LPS-induced production of inflammatory mediators through the inhibition of p38, JNK and NF-<TEX>${\kappa}B$</TEX> activation. Taken together, these results could provide the evidence for the anti-inflammatory effects of LE. Therefore, LE may be a novel target in the management of inflammation and help to support a potential strategy for prevention and therapy of inflammatory diseases.