D(−)-Salicin inhibits the LPS-induced inflammation in RAW264.7 cells and mouse models

• D(−)-Salicin markedly decreased TNF-α, IL-1β and IL-6 concentrations and increased IL-10 concentration in vivo and in vitro.
• D(−)-Salicin suppressed the activation of MAPKs and NF-κB signaling pathways stimulated by LPS in mouse model.
• 3. In the mouse model of acute lung injury, histopathologic examination indicted that D(−)-Salicin suppressed edema induced by LPS.
• 4. D(−)-Salicin might be a potential therapeutic agent against inflammatory diseases.

D(−)-Salicin is a traditional medicine which has been known to exhibit anti-inflammation and other therapeutic activities. The present study aimed to investigate whether D(−)-Salicin inhibited the LPS-induced inflammation in vivo and in vitro. We evaluated the effect of D(−)-Salicin on cytokines (TNF-α, IL-1β, IL-6 and IL-10) in vivo and in vitro by enzyme-linked immunosorbent assay and signaling pathways (MAPKs and NF-κB) in vivo by Western blot. The results showed that D(−)-Salicin markedly decreased TNF-α, IL-1β and IL-6 concentrations and increased IL-10 concentration. In addition, western blot analysis indicated that D(−)-Salicin suppressed the activation of MAPKs and NF-κB signaling pathways stimulated by LPS. To examine whether D(−)-Salicin ameliorated LPS-induced lung inflammation, inhibitors of MAPKs and NF-κB signaling pathways were administrated intraperitoneally to mice. Interference with specific inhibitors revealed that D(−)-Salicin-mediated cytokine suppression was through MAPKs and NF-κB pathways. In the mouse model of acute lung injury, histopathologic examination indicted that D(−)-Salicin suppressed edema induced by LPS. So it is suggest that D(−)-Salicin might be a potential therapeutic agent against inflammatory diseases.