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.