Maresin 1 Mitigates Inflammatory Response and Protects Mice from Sepsis

被引:39
|
作者
Li, Ruidong [1 ]
Wang, Yaxin [2 ]
Ma, Zhijun [1 ]
Ma, Muyuan [1 ]
Wang, Di [1 ]
Xie, Gengchen [1 ]
Yin, Yuping [1 ]
Zhang, Peng [1 ]
Tao, Kaixiong [1 ]
机构
[1] Huazhong Univ Sci & Technol, Union Hosp, Tongji Med Coll, Dept Gen Surg, 1277 Jiefang Ave, Wuhan 430022, Peoples R China
[2] Huazhong Univ Sci & Technol, Union Hosp, Tongji Med Coll, Dept Anesthesia & Crit Care, 1277 Jiefang Ave, Wuhan 430022, Peoples R China
基金
中国国家自然科学基金;
关键词
CECAL LIGATION; LUNG INJURY; LIPOPOLYSACCHARIDE; INHIBITION; TISSUE; MODEL; SHOCK;
D O I
10.1155/2016/3798465
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Sepsis, frequently caused by infection of bacteria, is considered as an uncontrollable systematic inflammation response syndrome (SIRS). Maresin 1 (Mar1) is a new proresolving mediator with potent anti-inflammatory effect in several animal models. However, its effect in sepsis is still not investigated. To address this question, we developed sepsismodel in BALB/c mice by cecal ligation and puncture (CLP) with or without Mar1 treatment. Our data showed that Mar1 markedly improved survival rate and decreased the levels of proinflammatory cytokines in CLP mice such as interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), and interleukin-1 beta (IL-1 beta). Furthermore, Mar1 reduced serum level of lipopolysaccharide (LPS) and enhanced the bacteria clearance in mice sepsis model. Moreover, Mar1 attenuated lung injury and decreased level of alanine transaminase (ALT), aspartate transaminase (AST), creatinine (Cre), and blood urea nitrogen (BUN) in serum in mice after CLP surgery. Treatment with Mar1 inhibited activation of nuclear factor kappa B (NF-kappa b) pathway. In conclusion, Mar1 exhibited protective effect in sepsis by reducing LPS, bacteria burden in serum, inhibiting inflammation response, and improving vital organ function. The possible mechanism is partly involved in inhibition of NF-kappa b activation.
引用
收藏
页数:9
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