Objective: Long non-coding RNAs (lncRNAs) are theorized to serve a critical role in cerebral ischemia/reperfusion injury. The purpose of this study was to determine whether knockdown of lncRNA SNHG1 protected against oxygen-glucose deprivation/reperfusion (OGD/R)-induced cell death in vitro and to investigate the underlying mechanisms. Methods: The expression levels of SNHG1 and miR-424 were detected by RT-qPCR analysis. The expression levels of apoptosis-related proteins were detected by western blot analysis. Cell viability and apoptosis were detected by MTT assay and flow cytometric analysis, respectively. Bioinformatic prediction and dual-luciferase reporter assay were performed to study the interaction between SNHG1 and miR-424. Results: The results showed that SNHG1 expression level was increased in OGD/R-treated SH-SY5Y cells, and knockdown of SNHG1 alleviates OGD/R-induced apoptosis and mitochondrial dysfunction in SH-SY5Y cells. Moreover, we found that SNHG1 might serve as a ceRNA for miR-424 in SH-SY5Y cells, and rescue experiments further confirmed that miR-424 inhibitor blocked the beneficial role of SNHG1 knockdown in OGD/R-treated SH-SY5Y cells. Conclusion: Taken together, this research supported the first evidence that lncRNA SNHG1 regulates OGD/R-induced cell death through serving as a ceRNA for miR-424 in SH-SY5Y cells.
Keywords: apoptosis; lncRNA SNHG1; miR-424; mitochondrial dysfunction; oxygen-glucose deprivation/reperfusion.