Accumulating studies have suggested the important role of microRNA (miRNA) in ischemic cerebral infarction. However, little is known of the modifying effect of miR-5787, a newly found miRNA, in ischemic cerebral infarction. We aim to elucidate the effect and underlying molecular mechanism of miR-5787 in the pathogenesis of ischemic cerebral infarction. MiR-5787 is demonstrated to be downregulated in peripheral blood mononuclear cells (PBMCs) samples of patients compared with controls, which is negatively associated with inflammatory cytokines of IL-6 and TNF-α in ischemic cerebral infarction. Besides, the expression of miR-5787 is also negatively related to TLR4, which is unregulated in PBMCs of ischemic cerebral infarction patients. Moreover, TLR4 is demonstrated to be a target of miR-5787 by bioinformatics’ analysis and the luciferase reporter assay. In addition, miR-5787 can prevent from the proliferation and migration of macrophages, and attenuate LPS/TLR4-mediated inflammatory response via NF-κB in macrophages. MiR-5787 may be a promising biomarker for ischemic cerebral infarction.

越来越多的研究表明microRNA（miRNA）在缺血性脑梗死中的重要作用。然而，关于 miR-5787（一种新发现的 miRNA）在缺血性脑梗死中的修饰作用知之甚少。我们旨在阐明 miR-5787 在缺血性脑梗死发病机制中的作用和潜在的分子机制。与对照组相比，MiR-5787 在患者的外周血单个核细胞 (PBMC) 样本中被证明下调，这与缺血性脑梗死中的炎症细胞因子 IL-6 和 TNF-α 呈负相关。此外，miR-5787的表达也与TLR4呈负相关，而TLR4在缺血性脑梗死患者的PBMC中不受调控。而且，通过生物信息学分析和荧光素酶报告基因分析，TLR4 被证明是 miR-5787 的靶标。此外，miR-5787 可以阻止巨噬细胞的增殖和迁移，并通过巨噬细胞中的 NF-κB 减弱 LPS/TLR4 介导的炎症反应。MiR-5787 可能是缺血性脑梗死的一个有前途的生物标志物。