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

水杨酸 体内 炎症 药理学 免疫印迹 医学 化学 生物 生物化学 免疫学 基因 生物技术
作者
Yang Li,Qianchao Wu,Yanhong Deng,Hongming Lv,Jiaming Qiu,Gefu Chi,Haihua Feng
出处
期刊:International Immunopharmacology [Elsevier]
卷期号:26 (2): 286-294 被引量:36
标识
DOI:10.1016/j.intimp.2015.04.016
摘要

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.
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