1. Academic Validation
  2. D(-)-Salicin inhibits the LPS-induced inflammation in RAW264.7 cells and mouse models

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

  • Int Immunopharmacol. 2015 Jun;26(2):286-94. doi: 10.1016/j.intimp.2015.04.016.
Yang Li 1 Qianchao Wu 1 Yanhong Deng 1 Hongming Lv 1 Jiaming Qiu 1 Gefu Chi 2 Haihua Feng 3
Affiliations

Affiliations

  • 1 Key Laboratory of Zoonosis, Ministry of Education, College of Animal Science and Veterinary Medicine, Jilin University, Changchun, Jilin 130062, PR China.
  • 2 Department of Outpatient Clinic, the Affiliated Hospital of Inner Mongolia University for the Nationalities, Tongliao 028000, People's Republic of China. Electronic address: chilanfu333@163.com.
  • 3 Key Laboratory of Zoonosis, Ministry of Education, College of Animal Science and Veterinary Medicine, Jilin University, Changchun, Jilin 130062, PR China. Electronic address: fhh70@163.com.
Abstract

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.

Keywords

Acute lung injury; Cytokines; D(−)-salicin; MAPK; NF-κB.

Figures
Products