Lixisenatide ameliorated lipopolysaccharide (LPS)‐induced expression of mucin and inflammation in bronchial epithelial cells

利西塞纳泰德 粘蛋白 脂多糖 炎症 化学 肿瘤坏死因子α 内科学 内分泌学 医学 生物化学 艾塞那肽 糖尿病 2型糖尿病
作者
Leiming Xu,Guoping Chen,Leiming Zhang,Aifeng He,Y Li
出处
期刊:Journal of Biochemical and Molecular Toxicology [Wiley]
卷期号:38 (1) 被引量:1
标识
DOI:10.1002/jbt.23618
摘要

Abstract Chronic obstructive pulmonary disease (COPD) induces serious social and economic burdens due to its high disability and mortality, the pathogenesis of which is highly involved with inflammation, oxidative stress (OS), and mechanism of mucin 5AC (MUC5AC) secretion. Lixisenatide is a selective glucagon‐like peptide 1 receptor agonist recently reported to have anti‐inflammatory properties. Our study will focus on the potential impact of lixisenatide on lipopolysaccharide (LPS)‐induced mucin secretion and inflammation in 16 human bronchial epithelial (16HBE) cells to check its potential function in COPD. 16HBE cells were treated with LPS, with or without lixisenatide (10 and 20 nM) for 1 day. Remarkably declined cell viability, enhanced lactate dehydrogenase release, activated OS, and elevated release of inflammatory cytokines were observed in LPS‐treated 16HBE cells, accompanied by the activation of nuclear factor‐κB signaling, all of which were signally reversed by lixisenatide. Moreover, elevated expression and release of MUC5AC were observed in LPS‐treated 16HBE cells but were markedly repressed by lixisenatide. Furthermore, the repressed nuclear factor erythroid 2‐related factor 2 (Nrf2) level in LPS‐treated 16HBE cells was notably rescued by lixisenatide. Lastly, following the knockdown of Nrf2, the protective function of lixisenatide on LPS‐triggered MUC5AC release in 16HBE cells was significantly abrogated. Collectively, lixisenatide ameliorated LPS‐induced expression of mucin and inflammation in bronchial epithelial cells by regulating Nrf2.
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