Format

Send to

Choose Destination
Int Immunopharmacol. 2015 Jun;26(2):286-94. doi: 10.1016/j.intimp.2015.04.016. Epub 2015 Apr 20.

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

Author information

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

PMID:
25907238
DOI:
10.1016/j.intimp.2015.04.016
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center