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The anti-inflammatory effect and mechanism of Usnic acid (UA) were explored on lipopoly-saccharide (LPS)-stimulated RAW264.7 cell line.The effects of UA on pro-inflammatory cytokines including tumor necrosis factor-alfa (TNF-α),interleukin-6 (IL-6) and interleukin-1 beta (IL-1β),pro-inflammatory mediators such as nitric oxide (NO),inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) were studied by sandwich ELISA,real-time PCR and western blot analyses.Similarly,the effect of UA on anti-inflammatory cytokine interleukin-10 (IL-10) and anti-inflammatory mediator heme oxygenase-1 (HO-1) were also studied following the same methods.Furthermore,nuclear factor-κB (NF-κB) was assayed by immunocytochemistry.The results showed that UA has anti-inflammatory effect by down-regulatinng iNOS,COX-2,IL-1β,IL-6 and TNF-α,COX-2 gene expression through the suppression of NF-κB activation and increasing anti-inflammatory cytokine IL-10 and anti-inflammatory mediator HO-1 production.
The anti-inflammatory effect and mechanism of Usnic acid (UA) were explored on lipopoly-saccharide (LPS) -stimulated RAW264.7 cell line. These effects of UA on pro-inflammatory cytokines including tumor necrosis factor-alfa (TNF- , interleukin-6 (IL-6) and interleukin-1 beta (IL-1β), pro- inflammatory mediators such as nitric oxide (NO), inducible nitric oxide synthase (iNOS) and cyclooxygenase- 2 by sandwich ELISA, real-time PCR and western blot analyzes. Similarly, the effect of UA on anti-inflammatory cytokine interleukin-10 (IL-10) and anti-inflammatory mediator heme oxygenase-1 the same methods. Frthermore, NF-κB was assayed by immunocytochemistry. The results showed that UA has anti-inflammatory effect by down-regulatinng iNOS, COX-2, IL-1β, IL-6 and TNF- α, COX-2 gene expression through the suppression of NF-κB activation and increasing anti-inflammatory cytokine IL-10 and anti-inflammatory mediator HO-1 production .