基因敲除
炎症
炎症体
硒缺乏症
小RNA
细胞凋亡
下调和上调
信使核糖核酸
受体
生物
细胞生物学
化学
癌症研究
免疫学
内科学
内分泌学
氧化应激
医学
基因
生物化学
超氧化物歧化酶
谷胱甘肽过氧化物酶
作者
Qing Zhang,Kaixin Zhang,Yanfei Han,Yiming Zhang,Xue Hua,Ling Zhou,Guangliang Shi,Shu Li
摘要
Abstract Selenium (Se) is an essential trace element in organism. Se deficiency can cause many diseases, including vascular disease. Studies have shown that inflammation is the main inducement of vascular disease, microRNA (miRNA) can influence inflammation in various ways, and Se deficiency can affect miRNAs expression. To study the mechanism of aorta damage caused by Se deficiency, we constructed a Se deficiency porcine aorta model and found that Se deficiency can significantly inhibit miR‐223, which downregulates the expression of nucleotide‐binding oligomerization domain‐like receptor family 3 (NLRP3). Subsequently, we found that in Se deficiency group, NLRP3, and its downstream (caspase‐1, apoptosis‐related spot‐like protein [ASC], IL‐18, IL‐1β) expression was significantly increased. In vitro, we cultured pig iliac endothelium cell lines, and constructed miR‐223 knockdown and overexpression models. NLRP3 messenger RNA and protein levels were significant increased in the knockdown group, and decreased in the overexpression group. The results of this study show that Se deficiency in porcine arteries can induce inflammation through miR‐223/NLRP3.
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