Abstract
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‑α, interleukin (IL)‑1β, 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)‑κB 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‑κB 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‑κB pathway suppression.