Next Article in Journal
Bee Venom Inhibits Porphyromonas gingivalis Lipopolysaccharides-Induced Pro-Inflammatory Cytokines through Suppression of NF-κB and AP-1 Signaling Pathways
Next Article in Special Issue
Impact of Cluster Zone Leaf Removal on Grapes cv. Regent Polyphenol Content by the UPLC-PDA/MS Method
Previous Article in Journal
Double Intramolecular Transacetalization of Polyhydroxy Acetals: Synthesis of Conformationally-Restricted 1,3-Dioxanes with Axially-Oriented Phenyl Moiety
Previous Article in Special Issue
Isobutylhydroxyamides from Zanthoxylum bungeanum and Their Suppression of NO Production
Article Menu
Issue 11 (November) cover image

Export Article

Open AccessArticle
Molecules 2016, 21(11), 1490;

Salidroside Regulates Inflammatory Response in Raw 264.7 Macrophages via TLR4/TAK1 and Ameliorates Inflammation in Alcohol Binge Drinking-Induced Liver Injury

Key Laboratory for Natural Resource of ChangBai Mountain & Functional Molecules, Ministry of Education, College of Pharmacy, Yanbian University, Yanji 133002, China
Clinical Research Center, Yanbian University Hospital, Yanji 133002, China
These authors contribute equally to this work.
Authors to whom correspondence should be addressed.
Academic Editor: Nancy D. Turner
Received: 27 September 2016 / Revised: 3 November 2016 / Accepted: 4 November 2016 / Published: 9 November 2016
(This article belongs to the Collection Bioactive Compounds)
Full-Text   |   PDF [3938 KB, uploaded 9 November 2016]   |  


The current study was designed to investigate the anti-inflammatory effect of salidroside (SDS) and the underlying mechanism by using lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages in vitro and a mouse model of binge drinking-induced liver injury in vivo. SDS downregulated protein expression of toll-like receptor 4 (TLR4) and CD14. SDS inhibited LPS-triggered phosphorylation of LPS-activated kinase 1 (TAK1), p38, c-Jun terminal kinase (JNK), and extracellular signal-regulated kinase (ERK). Degradation of IκB-α and nuclear translocation of nuclear factor (NF)-κB were effectively blocked by SDS. SDS concentration-dependently suppressed LPS mediated inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) protein levels, as well as their downstream products, NO. SDS significantly inhibited protein secretion and mRNA expression of of interleukin (IL)-1β and tumor necrosis factor (TNF)-α. Additionally C57BL/6 mice were orally administrated SDS for continuous 5 days, followed by three gavages of ethanol every 30 min. Alcohol binge drinking caused the increasing of hepatic lipid accumulation and serum transaminases levels. SDS pretreatment significantly alleviated liver inflammatory changes and serum transaminases levels. Further investigation indicated that SDS markedly decreased protein level of IL-1β in serum. Taken together, these data implied that SDS inhibits liver inflammation both in vitro and in vivo, and may be a promising candidate for the treatment of inflammatory liver injury. View Full-Text
Keywords: salidroside; inflammation; alcoholic liver injury; TLR4; TAK1 salidroside; inflammation; alcoholic liver injury; TLR4; TAK1

Graphical abstract

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).

Share & Cite This Article

MDPI and ACS Style

Sun, P.; Song, S.-Z.; Jiang, S.; Li, X.; Yao, Y.-L.; Wu, Y.-L.; Lian, L.-H.; Nan, J.-X. Salidroside Regulates Inflammatory Response in Raw 264.7 Macrophages via TLR4/TAK1 and Ameliorates Inflammation in Alcohol Binge Drinking-Induced Liver Injury. Molecules 2016, 21, 1490.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics



[Return to top]
Molecules EISSN 1420-3049 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top