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.

中文翻译：

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Omentin-1通过抑制TLR4 / MyD88 /NF-κB信号传导减弱脂多糖（LPS）诱导的U937巨噬细胞的活化。

巨噬细胞通过释放各种促炎介质，在抵抗有害病原体和刺激的防御反应中起关键作用。但是，促炎性介质的过量生产会对有机体造成伤害并引起与炎症相关的疾病。Omentin-1是一种新发现的脂肪因子，在网膜脂肪组织中特异性表达。最近的研究发现omentin-1与胰岛素抵抗，糖尿病，肥胖，炎症，动脉粥样硬化，骨代谢和肿瘤细胞增殖之间存在相关性。一些研究表明，omentin-1，胰岛素抵抗和炎症之间的关系可能表明omentin-1在慢性炎症性疾病中起重要作用。在这项研究中，我们发现omentin-1抑制LPS诱导巨噬细胞中炎症介质和促炎细胞因子的表达。此外，omentin-1通过抑制核p65积累和转染的NFκB启动子活性来抑制NF-κB通路的激活。重要的是，omentin-1增加了Nrf2的核易位。我们的发现表明omentin-1对LPS诱导的巨噬细胞具有抗炎作用，并且在与炎症相关的疾病的治疗中具有潜在的意义。