Omentin-1 attenuates lipopolysaccharide (LPS)-induced U937 macrophages activation by inhibiting the TLR4/MyD88/NF-κB signaling.

Abstract:

:Macrophages play a pivotal role in the defense response against harmful pathogens and stimuli by releasing various pro-inflammatory mediators. However, overproduction of pro-inflammatory mediators will do harm to the organism and cause inflammation-associated diseases. Omentin-1, which is a newly discovered adipokine, is specifically expressed in omental adipose tissue. Recent studies have found correlations between omentin-1 and insulin resistance, diabetes, obesity, inflammation, atherosclerosis, bone metabolism, and tumor cell proliferation. Some studies have shown that the association between omentin-1, insulin resistance, and inflammation might suggest that omentin-1 plays an important role in chronic inflammatory diseases. In this study, we found that omentin-1 inhibited LPS-induced expression of inflammatory mediators and pro-inflammatory cytokines in macrophages. Furthermore, omentin-1 inhibited activation of the NF-κB pathway by suppressing both nuclear p65 accumulation and transfected NFκB promoter activity. Importantly, omentin-1 increased nuclear translocation of Nrf2. Our findings demonstrate that omentin-1 exerts anti-inflammatory effects on LPS-induced macrophages and has potential implication in the treatment of inflammation-associated diseases.

journal_name

Arch Biochem Biophys

authors

Wang J,Gao Y,Lin F,Han K,Wang X

doi

10.1016/j.abb.2019.108187

subject

Has Abstract

pub_date

2020-01-15 00:00:00

pages

108187

eissn

0003-9861

issn

1096-0384

pii

S0003-9861(19)30791-X

journal_volume

679

pub_type

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