Objective: The roles of long non-coding RNA (lncRNAs) in ischemic stroke (IS) have been widely illustrated. Here, we focused on the function and mechanism of lncRNA SNHG7  in IS.
Methods: Middle cerebral artery occlusion (MCAO) was used for inducing mice  to establish IS models in vivo. Oxygen and glucose deprivation/reoxygenation (OGD/R) was used for treating PC12 cells to establish IS models in vitro. Relative expression of SNHG7  and miR-9  was determined by qRT-PCR. The neuronal injury was assessed by measuring relative activity of ROS, malondialdehyde (MDA) level and cell viability. Cell viability was determined by MTT assay. Dual-luciferase reporter (DLR) assay was employed to test the target of SNHG7  or miR-9 . Western blot was used to determine the protein expression of SIRT1 . Apoptosis rate was measured by flow cytometry.
Results: SNHG7  was down-regulated and miR- 9 was up-regulated by MCAO treatment in brain tissues of mice  and by OGD/R treatment in PC12 cells. Overexpression of SNHG7  or suppression of miR-9  decreased the relative activity of ROS and the MDA level as well as enhancing cell viability, and SNHG7  reduced apoptosis rate in OGD/R-induced PC12 cells (IS cells). MiR-9  was targeted by SNHG7  and SIRT1  was targeted by miR-9 . The protein expression of SIRT1  was reduced by OGD/R treatment in PC12 cells. The suppressive effects of SNHG7  on the relative activity of ROS, the MDA level and apoptosis rate as well as the promotion effect of SNHG7  on cell viability were reversed by miR-9  mimics or sh-SIRT1  in IS cells.
Conclusion: LncRNA SNHG7  alleviated OGD/R-induced neuronal injury by mediating miR-9 /SIRT1  axis in vitro.
Keywords: ischemic stroke, oxygen and glucose deprivation/reoxygenation, small nucleolar RNA host gene 7, miR-9, silent information regulator factor 2-related enzyme 1