MicroRNA-22 alleviates inflammation in ischemic stroke via p38 MAPK pathways

The present study aimed to ascertain the potential roles and mechanisms of action of micro (mi)RNA-22 in ischemic stroke. The results indicated that miRNA-22 expression was downregulated in ischemic stroke rats model, compared with a control group. The downregulation of miRNA-22 upregulated the expression of inflammatory factors [including tumor necrosis factor-alpha, interleukin (IL)-1 beta, IL-6 and IL-18]. It could also induce the expression of macrophage inflammatory protein (MIP-2), prostaglandin E2 (PGE2), cyclooxygenase-2 (COX-2) and inducible NO synthase (iNOS) in the in vitro model. By contrast, the overexpression of miRNA-22 downregulated the expression of inflammatory factors, and suppressed the expression of MIP-2, PGE2, COX-2 and iNOS in the in vitro model. The downregulation of miRNA-22 induced the protein expression of nuclear factor (NF)-kappa B and phosphorylated-p38 (p-p38) mitogen-activated protein kinase (MAPK) in the in vitro model. By comparison, the overexpression of miRNA-22 suppressed the protein expression of NF-kappa B and p-p38 in the in vitro model. Typically, LY2228820, the p38 inhibitor (3 nM) would mitigate the pro-inflammatory effects of anti-miRNA-22 in the in vitro model. These results suggested that miRNA-22 can alleviate ischemic stroke-induced inflammation in rats model or vitro model through p38 MAPK/NF-kappa B pathway suppression.