miRNA-20b inhibits cerebral ischemia-induced inflammation through targeting NLRP3

The present study was designed to investigate the role of microRNA (miRNA)-20b in the inflammatory response during cerebral ischemia and the underlying mechanism following cerebral ischemia. A reverse transcription quantitative polymerase chain reaction assay was used to measure the expression of miRNA-20b, and tumor necrosis factor α, interleukin (IL)-6, IL-18 and IL-1β levels were measured using ELISA. In addition, the protein expression levels of NOD-like receptor pyrin domain containing 3 (NLRP3), caspase-1, IL-1β and IL-18 were determined by western blot analysis. It was determined that the expression of miRNA-20b during cerebral ischemia was increased compared with the control group. The overexpression of miRNA-20b increased the levels of IL-1β and IL-18 in the cerebral ischemia group through activation of the NLRP3 signaling pathway. Conversely, the downregulation of miRNA-20b suppressed IL-1β and IL-18 levels in cerebral ischemia via suppression of the NLRP3 signaling pathway. Additionally, the overexpression of miRNA-20b increased the levels of adenosine 5′-triphosphate (ATP) and reactive oxygen species (ROS) in the cerebral ischemia group, which were decreased following the downregulation of miRNA-20b. The inhibition of NLRP3 decreased the pro-inflammatory effects of miRNA-20b in cerebral ischemia. Suppression of ATP decreases the pro-inflammatory effects of miRNA-20b in cerebral ischemia. Suppression of ROS also decreases the pro-inflammatory effects of miRNA-20b in cerebral ischemia. Collectively, the present study provided novel insight into the role of miRNA-20b upregulation in the promotion of inflammation following cerebral infarction, suggesting that the miRNA-20b/NLRP3 axis may be a putative therapeutic target in cerebral ischemia.