Carvacrol protects mice against LPS-induced sepsis and attenuates inflammatory response in macrophages by modulating the ERK1/2 pathway

被引:12
|
作者
Yan, Chenghua [1 ]
Kuang, Wendong [2 ,3 ]
Jin, Liang [2 ]
Wang, Rongliang [1 ]
Niu, Ling [1 ]
Xie, Chuanqi [4 ]
Ding, Jian [5 ]
Liao, Yongcui [1 ]
Wang, Liyuan [1 ]
Wan, Hongjiao [1 ]
Ma, Guangqiang [1 ]
机构
[1] Jiangxi Univ Chinese Med, Coll Tradit Chinese Med, Coll Life Sci, Nanchang 330004, Peoples R China
[2] Jiangxi Acad Sci, Inst Microbiol, Nanchang 330029, Peoples R China
[3] State Key Lab Virol, Wuhan 430071, Peoples R China
[4] Jiangxi Acad Sci, Inst Appl Chem, Nanchang 330029, Peoples R China
[5] Nanchang Univ, Affiliated Hosp 1, Nanchang 330006, Peoples R China
基金
中国国家自然科学基金;
关键词
ACTIVATION; INJURY; SHOCK;
D O I
10.1038/s41598-023-39665-7
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Macrophages play an important role in the development of life-threatening sepsis, which is characterized by multiorgan dysfunction, through their ability to produce inflammatory cytokines. Carvacrol is a phenolic compound that has been confirmed to possess strong anti-inflammatory activity. In this study, we mainly investigated the effect of carvacrol on lipopolysaccharide (LPS)-induced macrophage proinflammatory responses and endotoxic shock. The results showed that carvacrol significantly reduced mouse body weight loss and ameliorated pathological damage to the liver, lung, and heart under LPS-induced sepsis. Carvacrol attenuated inflammatory responses by inhibiting the LPS-induced production of inflammatory cytokine interleukin-6 (IL-6) in vivo and in vitro. Mechanistically, carvacrol inhibited IL-6 production mainly through the ERK1/2 signalling pathway in macrophages. Furthermore, carvacrol improved the survival of septic mice. This study sheds light on the role of carvacrol in the pathogenesis of LPS-induced sepsis, and thus, its potential in treating sepsis patients may be considered.
引用
收藏
页数:10
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