Molecular mechanisms of the anti-inflammatory effect of sinomenine on atopic dermatitis

摘要

Sinomenine (SIN) is the major bioactive component of the Chinese medicinal herb Sinomenium acutum and its anti-inflammatory effects are well established. The purpose of this study was to investigate the effect of SIN on the progression of atopic dermatitis (AD) in vitro, and explore the underlying molecular mechanisms. A cell model of AD was established by stimulating RAW264.7 cells with 1 mu g/ml LPS. The cells were treated with different concentrations of SIN (0.25, 0.5 or 1 mM), and cell viability was analyzed by MTT assay. The levels of the pro-inflammatory cytokines interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) were measured by ELISA. Furthermore, NO production in RAW264.7 cells was detected using the nitrate/nitrite assay kit, and the related gene and protein expression levels were determined by qRT-PCR or/and western blot, respectively. SIN inhibited LPS induced increase in the level of proinflammatory cytokines (TNF alpha, IL-1 beta and IL-6) and NO production in a dose-dependent manner. LPS increased the expression levels of iNOS and COX2, while pretreatment with SIN markedly decreased iNOS and COX2 expression. Moreover, LPS-induced activation of p38MAPK-NF-kappa B pathways was suppressed by SIN. Our results demonstrated the anti-inflammatory effect of SIN on AD via regulating the p38MAPK-NF-kappa B pathway.