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Long Non-Coding RNA SNHG7 Alleviates Oxygen and Glucose Deprivation/Reoxygenation-Induced Neuronal Injury by Modulating miR-9/SIRT1 Axis in PC12 Cells: Potential Role in Ischemic Stroke

Authors Zhou T, Wang S, Lu K, Yin C

Received 22 July 2020

Accepted for publication 19 October 2020

Published 24 November 2020 Volume 2020:16 Pages 2837—2848


Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Dr Jun Chen

Tao Zhou,1,* Shuai Wang,1,* Kai Lu,2 Chunhui Yin3

1Department of Neurosurgery, Zibo First Hospital, Zibo City 255200, People’s Republic of China; 2Department of Neurology, Liaocheng Third People’s Hospital, Liaocheng City 252000, People’s Republic of China; 3Department of Intervention Clinic, Weifang Hospital of Traditional Chinese Medicine, Weifang City 261000, People’s Republic of China

*These authors contributed equally to this work

Correspondence: Chunhui Yin
Department of Intervention Clinic, Weifang Hospital of Traditional Chinese Medicine, No. 1055, Weizhou Road, Kuiwen District, Weifang City, Shandong Province 261000, People’s Republic of China
Tel +86- 0536-8190000

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

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