Salidroside attenuates LPS-induced pro-inflammatory cytokine responses and improves survival in murine endotoxemia

• Published in: International immunopharmacology 2011-12, Vol.11 (12), p.2194-2199
• Main Authors: Guan, Shuang, Feng, Haihua, Song, Bocui, Guo, Weixiao, Xiong, Ying, Huang, Guoren, Zhong, Weiting, Huo, Meixia, Chen, Na, Lu, Jing, Deng, Xuming
• Format: Article
• Language: English
• Subjects: Animals; Anti-Inflammatory Agents - therapeutic use; Biological and medical sciences; Cell Line; Cytokines; Cytokines - biosynthesis; Down-Regulation - drug effects; Endotoxemia; Endotoxemia - chemically induced; Endotoxemia - drug therapy; ERK/MAPKs; Glucosides - therapeutic use; Inflammation - chemically induced; Inflammation - drug therapy; Lipopolysaccharides - administration & dosage; Macrophages - drug effects; Male; MAP Kinase Signaling System - drug effects; Medical sciences; Mice; Mice, Inbred C57BL; NF-kappa B - metabolism; NF-қB; Pharmacology. Drug treatments; Phenols - therapeutic use; Salidroside; Treatment Outcome
• ISSN: 1567-5769; 1878-1705
• DOI: 10.1016/j.intimp.2011.09.018

Salidroside is a major component isolated from the Rhodiola rosea. In the present study, we investigated the anti-inflammatory effects of salidroside on cytokine production by lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages in vitro, and the results showed that salidroside reduced tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and interleukin-1β (IL-1β) secretions. This inspired us to further study the effects of salidroside in vivo. Salidroside significantly attenuated TNF-α, IL-1β and IL-6 productions in serum from mice challenged with LPS, and consistent with the results in vitro. In the murine model of endotoxemia, mice were treated with salidroside prior to or after LPS challenge. The results showed that salidroside significantly increased mouse survival. Further studies revealed that salidroside could downregulate LPS-induced nuclear transcription factor-қB (NF-қB) DNA-binding activation and ERK/MAPKs signal transduction pathways production in RAW 264.7 macrophages. These observations indicated that salidroside modulated early cytokine responses by blocking NF-қB and ERK/MAPKs activation, and thus, increased mouse survival. These effects of salidroside may be of potential usefulness in the treatment of inflammation-mediated endotoxemia. ► Salidroside reduced TNF-α, IL-6 and IL-1β secretions from LPS-stimulated RAW 264.7 macrophages in vitro. ► Salidroside attenuated TNF-α, IL-1β and IL-6 productions in serum from mice challenged with LPS. ► Salidroside increased survival rate of mouse treated with salidroside prior to or after LPS challenge. ► Salidroside modulated cytokine responses by blocking NF-қB and ERK/MAPKs activation.