Background: Ischemia/reperfusion (I/R) injury involves complex biological processes
and molecular mechanisms such as autophagy. Oxidative stress plays a critical role in the pathogenesis
of I/R injury. LncRNAs are the regulatory factor of cerebral I/R injury.
Methods: This study constructs cerebral I/R model to investigate role of autophagy and oxidative
stress in cerebral I/R injury and the underline regulatory mechanism of SIRT1/ FOXO3a pathway.
In this study, lncRNA SNHG12 and FOXO3a expression was up-regulated and SIRT1 expression
was down-regulated in HT22 cells of I/R model.
Results: Overexpression of lncRNA SNHG12 significantly increased the cell viability and inhibited
cerebral ischemicreperfusion injury induced by I/Rthrough inhibition of autophagy. In addition,
the transfected p-SIRT1 significantly suppressed the release of LDH and SOD compared with cells
co-transfected with SIRT1 and FOXO3a group and cells induced by I/R and transfected with p-SNHG12
group and overexpression of cells co-transfected with SIRT1 and FOXO3 further decreased
the I/R induced release of ROS and MDA.
Conclusion: In conclusion, lncRNA SNHG12 increased cell activity and inhibited oxidative stress
through inhibition of SIRT1/FOXO3a signaling-mediated autophagy in HT22 cells of I/R model.
This study might provide new potential therapeutic targets for further investigating the mechanisms
in cerebral I/R injury and provide.