College of Animal Science,Southwest University, Rongchang, Chongqing 402460,China.
College of Animal Science,Southwest University, Rongchang, Chongqing 402460,China.
Neurosci Lett. 2020 Apr 23;725:134902. doi: 10.1016/j.neulet.2020.134902. Epub 2020 Mar 9.
Oxidative stress is implicated in the initiation and progression of human and animal diseases. MicroRNA (MiR) has been reported to be involved in the body's regulation to oxidative stress. We investigated if miR-183 regulates lipopolysaccharide (LPS)-induced oxidative stress in the hippocampus of weaned piglets. LPS-treated piglets had lower expression of miR-183 and higher expression of the fibronectin(FN)1 gene in their hippocampus than control piglets. The expression profiles of miR-183 and the FN1 gene in primary cultured rat hippocampal neurons exposed to LPS were consistent with those in the hippocampus of LPS-treated piglets. The LPS-induced expression of FN1 was reversed in hippocampal neurons by transfection with an miR-183 mimic. A luciferase reporter assay further demonstrated that the FN1 gene is a direct target of miR-183. Taken together, our results demonstrated that miR-183 regulates LPS-induced oxidative stress at least in part by targeting FN1.
氧化应激与人类和动物疾病的发生和发展有关。已有报道称，微小 RNA（miRNA）参与了机体对氧化应激的调节。我们研究了 miR-183 是否调节断奶仔猪海马中的脂多糖（LPS）诱导的氧化应激。与对照组仔猪相比，LPS 处理的仔猪海马中 miR-183 的表达降低，纤连蛋白（FN）1 基因的表达升高。原代培养的大鼠海马神经元暴露于 LPS 后，miR-183 和 FN1 基因的表达谱与 LPS 处理的仔猪海马中的表达谱一致。用 miR-183 模拟物转染可逆转 LPS 诱导的 FN1 表达。荧光素酶报告基因检测进一步表明 FN1 基因是 miR-183 的直接靶基因。综上所述，我们的研究结果表明，miR-183 通过靶向 FN1 来调节 LPS 诱导的氧化应激。
