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

被引:93
作者
Guan, Shuang [1 ,2 ]
Feng, Haihua [1 ]
Song, Bocui [1 ]
Guo, Weixiao [1 ]
Xiong, Ying [1 ]
Huang, Guoren [2 ]
Zhong, Weiting [1 ]
Huo, Meixia [1 ]
Chen, Na [1 ]
Lu, Jing [1 ,2 ]
Deng, Xuming [1 ]
机构
[1] Jilin Univ, Coll Anim Sci & Vet Med, Dept Vet Pharmacol, Changchun 130062, Jilin, Peoples R China
[2] Jilin Univ, Lab Nutr & Funct Food, Changchun 130062, Jilin, Peoples R China
关键词
Salidroside; Cytokines; Endotoxemia; NF-; B; ERK/MAPKs; RHODIOLA-ROSEA L; IN-VITRO; STRESS; SHOCK;
D O I
10.1016/j.intimp.2011.09.018
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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-alpha (TNF-alpha), interleukin-6 (IL-6) and interleukin-1 beta (IL-1 beta) secretions. This inspired us to further study the effects of salidroside in vivo. Salidroside significantly attenuated TNF-alpha, IL-1 beta 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- B (NF- B) 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- B 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. (C) 2011 Elsevier B.V. All rights reserved.
引用
收藏
页码:2194 / 2199
页数:6
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