MicroRNA‑497 attenuates cerebral infarction in patients via the TLR4 and CREB signaling pathways.

Abstract

The aim of the present study was to investigate the function and mechanism of microRNA‑497 (miRNA/miR‑149) in the regulation of cerebral infarction. In patients with cerebral infarction, the serum of microRNA‑497 expression was upregulated compared with that in healthy controls. In N2A cells, overexpression of miR‑497 induced cell proliferation, decreased apoptosis and caspase‑3 and caspase‑9 activities, and suppressed Bax protein expression compared with that in the negative control group. Overexpression of miR‑497 reduced inflammation factors, and suppressed the Toll‑like receptor 4 (TLR4), myeloid differentiation primary response protein MyD88 (MyD88) and nuclear factor‑κB (NF‑κB) protein expression of the N2A cells. Next, miR‑497 overexpression suppressed the protein expression of interleukin‑1 receptor associated kinase (IRAK1) and phosphorylated cyclic AMP response element binding protein (p-CREB) in the N2A cells. Following miR‑497 overexpression, TLR4 inhibitor was found to suppress the inflammation factors, suppress the TLR4, MyD88 and NF‑κB protein expression, and reduce the IRAK1 and p‑CREB protein expression of the N2A cells. Lastly, CREB inhibitor also suppressed p‑CREB protein expression, induced cell proliferation, decreased apoptosis and caspase‑3 and caspase‑9 activities, and suppressed Bax protein expression in the N2A cells following miR‑497 overexpression. Taken together, these data demonstrated that miR‑497 attenuated cerebral infarction in patients by regulating the TLR4 and CREB signaling pathways.