Abstract
Indigofera suffruticosa Mill is used as an herbal medicine for the treatment of inflammation. The aim of this study is to assess the anti-inflammatory potency of I. suffruticosa and its likely molecular mechanisms of action in lipopolysaccharide (LPS)-induced RAW 264.7 macrophages. Both water and ethanolic extracts of I. suffruticosa significantly decreased LPS-induced nitric oxide (NO) as well as the expression of inducible nitric oxide synthase (iNOS), tumor necrosis factor-α, and pro-interleukin-1β. Moreover, LPS-induced inhibitory factor-κB-α phosphorylation, nuclear factor-κB (NF-κB) nuclear protein-DNA binding affinity, and NF-κB reporter gene activity were dramatically inhibited by I. suffruticosa extracts. Exogenous addition of I. suffruticosa significantly induced heme oxygenase-1 (HO-1) expression, and the presence of HO-1 small interfering RNA partly reversed the inhibitory effects of I. suffruticosa on LPS-induced NO production and iNOS expression. Furthermore, I. suffruticosa induced HO-1 expression may be through activation of the ERK/nuclear factor E2-related factor 2 pathway. Eight phenolic compounds were found in the I. suffruticosa extracts, but salicylic acid was the only one detected in the plasma of mice fed with I. suffruticosa extracts. In summary, I. suffruticosa have a strong anti-inflammatory property that diminishes pro-inflammatory mediator expressions by lessening LPS-induced NF-κB activation and inducing HO-1 expression in macrophages.
