Knockout of cytochrome P450 1A1 enhances lipopolysaccharide‐induced acute lung injury in mice by targeting NF‐κB activation
Author(s) -
Tian Lixing,
Tang Xin,
Ma Wei,
Wang Jing,
Zhang Wei,
Liu Kuan,
Chen Tao,
Zhu Junyu,
Liang Huaping
Publication year - 2020
Publication title -
febs open bio
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.718
H-Index - 31
ISSN - 2211-5463
DOI - 10.1002/2211-5463.12977
Subject(s) - lipopolysaccharide , lactate dehydrogenase , hyperoxia , nitric oxide , lung , creatine kinase , knockout mouse , nitric oxide synthase , inflammation , chemistry , medicine , pharmacology , endocrinology , biochemistry , enzyme , receptor
CYP1A1 was induced in lung of mice by LPS treatment with an aryl hydrocarbon receptor‐independent manner, while Toll‐like receptor 4 knockout abolished CYP1A1 overexpression. CYP1A1 deficiency elevated pro‐inflammatory cytokines in lung tissues of septic mice by targeting NF‐κB (p65) and increased lung injury in response to LPS or E . coli challenge.
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