Salidroside attenuates LPS-stimulated activation of THP-1 cell-derived macrophages through down-regulation of MAPK/NF-kB signaling pathways.
10.1007/s11596-013-1143-6
- Author:
Hong-wu WANG
1
;
Ting WU
;
Jun-ying QI
;
Ya-qi WANG
;
Xiao-ping LUO
;
Qin NING
Author Information
1. Department of Infectious Disease, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China, hongwuwang@126.com.
- Publication Type:Journal Article
- MeSH:
Cell Line;
Down-Regulation;
drug effects;
genetics;
immunology;
Glucosides;
pharmacology;
Humans;
Lipopolysaccharides;
immunology;
Macrophages;
drug effects;
immunology;
Mitogen-Activated Protein Kinases;
genetics;
NF-kappa B;
genetics;
Phenols;
pharmacology;
Signal Transduction;
drug effects;
genetics;
immunology
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2013;33(4):463-469
- CountryChina
- Language:English
-
Abstract:
Excessive activation of macrophages is implicated in various inflammatory injuries. Salidroside (Sal), one of the main bioactive components of Rhodiola Sachalinensis, has been reported to possess anti-inflammatory activities. This study aimed to examine the effect of Sal on the activation of macrophages and the possible mechanism. The lipopolysaccharide (LPS)-stimulated phrobol 12-myristate 13-acetate (PMA)-differentiated THP-1 macrophage models were established. The changes in the inflammatory profiles of THP-1-derived macrophages were determined. The results showed that Sal significantly decreased the expression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX2), interleukin-1beta (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) at both mRNA and protein levels in THP-1-derived macrophages, and the effect was dose-depedent. Moreover, NF-κB activation was significantly suppressed and the phosphorylation of ERK, p38 and JNK was substantially down-regulated after Sal treatment. The findings suggested that Sal can suppress the activation of LPS-stimulated PMA-differetiated THP-1 cells, as evidenced by the decreased expression of iNOS, COX2, IL-1β, IL-6 and TNF-α, and the mechanism involves the inhibition of NF-κB activation and the phosphorylation of the MAPK signal pathway.
