Therapeutic effects of silibinin on LPS-induced acute lung injury by inhibiting NLRP3 and NF-κB signaling pathways

被引:42
作者
Tian, Lin [1 ]
Li, Weimin [2 ]
Wang, Tan [1 ]
机构
[1] Changchun Univ Chinese Med, Affiliated Hosp, Dept Respirol, Changchun 130000, Jilin, Peoples R China
[2] Changchun Univ Chinese Med, Affiliated Hosp, Encephalopathy Treatment Area, Changchun 130000, Jilin, Peoples R China
关键词
Silibinin; LPS; Lung injury; NLRP3; RESPIRATORY-DISTRESS-SYNDROME; INFLAMMASOME ACTIVATION; CYTOKINE PRODUCTION; TNF-ALPHA; RECEPTORS; EXPRESSION; SEPSIS; REPAIR; EDEMA; CELLS;
D O I
10.1016/j.micpath.2017.05.011
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Silibinin, a natural product extracted from Silybum marianum (milk thistle), has been reported to have anti-inflammatory effect. The aim of this study was to explore the therapeutic effects and potential mechanisms of silibinin on lipopolysaccharide (LPS)-stimulated inflammatory responses in acute lung injury (ALI). Male BALB/c mice were conditioned with silibinin 1 h after intranasal instillation of LPS. After 12 h, the myeloperoxidase (MPO) level in lung tissues, the wet/dry (W/D) ratio, inflammatory cytokines in the bronchoalveolar lavage fluid (BALF), and histopathological examination of lung were detected. Our results showed that silibinin inhibited LPS-induced histopathological changes and MPO activity, as well as the wet/dry (W/D) ratio in the lung tissues. Furthermore, silibinin significantly inhibited LPS-induced inflammatory cytokines production in the BALE. In addition, silibinin suppressed LPS-induced NF-x13 activation and the expression of NLRP3 inflammasome. These results indicate that silibinin exerts its anti-inflammatory effect by inhibiting NF-kappa B and NLRP3 signaling pathways. (C) 2017 Published by Elsevier Ltd.
引用
收藏
页码:104 / 108
页数:5
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