Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

MiR-16 exacerbates neuronal cell growth and inhibits cell apoptosis by targeting AKT3 in cerebral ischemia injury

Yijun Song¹ , Bo Wang²

¹Department of Internal Neurology; ²Department of Rehabilitation Medicine, Penglai Traditional Chinese Medicine Hospital of Yantai City, Yantai City 265600, China.

For correspondence:- Yijun Song Email: tuanyefu419794@163.com

Accepted: 24 September 2021 Published: 31 October 2021

Citation: Song Y, Wang B. MiR-16 exacerbates neuronal cell growth and inhibits cell apoptosis by targeting AKT3 in cerebral ischemia injury. Trop J Pharm Res 2021; 20(10):2049-2054 doi: 10.4314/tjpr.v20i10.6

© 2021 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To evaluate the role of miR-16 in ischemic neuronal injury.

Methods: An oxygen-glucose deprivation (OGD) model of ischemic neuronal injury was established in human brain cortical neuron HCN-2 cell line via hypoxic treatment. The mRNA or protein expressions of miR-16, AKT3, Bax and Bcl-2 were assessed by quantitative real time-polymerase chain reaction (qRT-PCR) or western blot assay. Targetscan online software was applied to predict potential targets of miR-16. Cell proliferation was measured by CCK-8 assay while the relationship between miR-16 and AKT3 was determined by Luciferase reporter assay.

Results: MiR-16 was overexpressed after OGD treatment. MiR-16 overexpression significantly promoted the proliferation of cortical neurons and inhibited their apoptosis, while miR-16 inhibition produced an opposite effect. The expression of AKT3 was increased after miR-16 inhibition, but it was decreased when miR-16 was overexpressed. In addition, luciferase reporter gene results showed that miR-16 targeted AKT3. Functional experiments showed that AKT3 overexpression reversed the effect of miR-16 overexpression on ischemic injury.

Conclusion: MiR-16 regulates neuronal cell growth and cell apoptosis through AKT3 expression. These results present new potential therapeutic targets for the treatment of cerebral ischemic stroke.

Keywords: Cerebral ischemic injury, Oxygen-glucose deprivation, miR-16, AKT3