Abstract
Ischemic stroke is a kind of disease with high mortality and high disability, which brings a huge burden to the public health system (Hu et al. (2017)), and it poses a serious threat to the quality of life of patients. Cerebral ischemia/reperfusion injury is an important pathophysiological mechanism. This study aims to assess the mechanism of SNHG15 in the occurrence and development of cerebral ischemia/reperfusion injury of nerve cells and to investigate its potential value for diagnosis and treatment. SNHG15 targeted miRNA molecules and target genes were predicted with bioinformatics tools such as StarBase and TargetScan. The process of ischemic reperfusion in cerebral apoplexy in normal cultured and oxygen-glucose-deprived and reoxygenated neurons was simulated with RT-PCR and western blot technique. The expressions of SNHG15 and miR-141 were detected with qPCR, and the expressions of SIRT1 and p65, TNF-α, ROS, iNOS, and IL-6 were detected with western blot. Meanwhile, SNHG15 siRNAs and miR-141 mimics were transfected for SH-SY5Y, with western blot testing. And the expressions of miR-141, SIRT1, and p65, TNF-α, ROS, iNOS, and IL-6 were tested. According to the prediction with bioinformatics tools of StarBase and TargetScan, miR-141 is the target of lncSNHG15. In the luciferase reporter plasmid double-luciferase assay, miR-141 and SIRT1 were defined as the target relationship. In the oxygen-glucose-deprived reoxygenation model group, SNHG15 expression increased, miR-141 expression decreased, SIRT1 expression increased, and the expressions of p65, TNF-α, ROS, iNOS, and IL-6 decreased. In the SNHG15-siRNA-transfected oxygen-glucose-deprived reoxygenation cell model group, miR-141 expression increased, SIRT1 expression decreased, and the expressions of p65, TNF-α, and IL-6 increased compared with the si-NC group. In the miR-141-mimic-transfected oxygen-glucose-deprived reoxygenation cell model, SNHG15 expression decreased, SIRT1 expression decreased, and the expressions of p65, TNF-α, IL-1β, and IL-6 increased. In conclusion, SNHG15 expression increased during the process of oxygen-glucose-deprived reoxygenation, and the oxidative stress process was reduced by miR-141/SIRT1.