circ_0000018 downregulation peripherally ameliorates neuroprotection against acute ischemic stroke through the miR‑871/BCL2L11 axis.

Acute ischemic stroke (AIS) is a common acute cerebrovascular disease. Circular RNAs (circRNAs) have been demonstrated to have critical functions in a wide range of physiological processes and disorders in humans. However, their precise function in ischemic stroke (IS) remains largely unknown. The present study explored the function and potential mechanisms of circ_0000018 in AIS in vivo and in vitro. The cerebral ischemia/reperfusion injury model was established in vivo and in vitro using the oxygen‑glucose deprivation (OGD/R) and transient middle cerebral artery occlusion (tMCAO) methods. Subsequently, the impact of circ_0000018 on cerebral ischemia/reperfusion injury was assessed using various techniques, including TTC staining, quantitative PCR, western blotting, cell counting kit‑8 assay, Annexin V‑FITC Apoptosis Detection Kit, luciferase reporter gene assays, and others. The levels of circ_0000018 were markedly increased in the OGD/R‑treated neuronal cells and in a mouse model of tMCAO. The blocking of microRNA (miR)‑871 by circ_0000018 promoted Bcl‑2‑like protein 11 (BCL2L11) expression to increase neuronal cell damage. Furthermore, circ_0000018 knockdown significantly improved neuronal cell viability and attenuated OGD/R‑treated neuronal cell death. Meanwhile, circ_0000018 knockdown improved brain infarct volume and neuronal apoptosis in tMCAO mice. The present study found that circ_0000018 knockdown relieved cerebral ischemia‑reperfusion injury progression in vitro and in vivo. Mechanistically, circ_0000018 regulated the levels of BCL2L11 by sponging miR‑871.