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Arch Biochem Biophys. 2019 Nov 7:108187. doi: 10.1016/j.abb.2019.108187. [Epub ahead of print]

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

Author information

1
Department of Critical Care Medicine, The Second Affiliated Hospital of Hainan Medical University, Haikou City, Hainan province, China.
2
Department of Infectious Disease, The Hainan Affiliated Hospital of Hainan Medical University, Haikou City, Hainan province, China.
3
Department of Critical Care Medicine, The Second Affiliated Hospital of Hainan Medical University, Haikou City, Hainan province, China. Electronic address: benjamint72@163.com.

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.

KEYWORDS:

Inflammation; LPS; Macrophage; NF-κB; Omentin-1

PMID:
31706880
DOI:
10.1016/j.abb.2019.108187

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