Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

LncRNA SNHG1 protects the cardiac muscle cells from hypoxia/ re-oxygenation injury in vitro by targeting microRNA-21-5p and miR-30a-5p

Youbin Liu¹, Tingting Zhang¹, Ying Fan¹, Jinglong Li¹, Meng Chen¹, Anyong Chen¹, Dahao Yang¹, Xue Guan², Yong Cao^1,3

¹Department of Cardiology, The second Affiliated Hospital of Harbin Medical University, Harbin, PR China; ²Department of Animal Center, The Second Affiliated Hospital of Harbin Medical University, Harbin, PR China; ³The Affiliated Hospital of Jining Medical University, Jining city, Shandon?272000, China.

For correspondence:- Yong Cao Email: trcv5645@126.com Tel:+8618273605524

Accepted: 26 April 2020 Published: 31 January 2021

Citation: Liu Y, Zhang T, Fan Y, Li J, Chen M, Chen A, et al. LncRNA SNHG1 protects the cardiac muscle cells from hypoxia/ re-oxygenation injury in vitro by targeting microRNA-21-5p and miR-30a-5p. Trop J Pharm Res 2021; 20(1):89-95 doi: 10.4314/tjpr.v20i1.14

© 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: Cardiovascular diseases are responsible for numerous deaths globally. Long noncoding RNA SNHG1 has presented its protective role in cardiomyocytes previously. Herein, we examined the underlying molecular mechanisms of SNHG1 in cardiac muscle cells from hypoxia and re-oxygenation (H/R) in vitro.

Methods: RT-qPCR measured expression of SNHG1, miR-21-5p and miR-30a-5p in rat cardiac muscle cell line HL-1 before and after H/R treatment and cell transfection, which was applied to regulate expression of SNHG1, miR-21-5p and miR-30a-5p for further use. The flow cytometry method was used to compare changes in cellular apoptosis, and cell viability was measured by CCK-8 method. Bioinformatics predicted the bindings ofSNHG1 and miR-21-5p / miR-30a-5p while the luciferase reporter assays further verified this.

Results: The outcomes revealedthat SNHG1 was downregulated and meanwhile miR-21-5p / miR-30a-5p was elevated that enhanced apoptosis and reduced cell viability in HL-1 cells. However, overexpressed SNHG1 inhibited cell apoptosis and increased cell viability brought by H/R. In addition, SNHG1 targeted at miR-21-5p/ miR-30a-5p, which contributed to the inter-regulation in between. Furthermore, interactive experiments revealed that upregulation of miR-21-5p/ miR-30a-5p added to the cell apoptosis which was induced by H/R and partially counteracted by the upregulation of SNHG1.

Conclusion: In this study we have demonstrated the protective role of SNHG1 in the moderation of H/R-induced HL-1 apoptosis and viability through suppression of miR-21-5p/miR-30a-5p. This offers new perspective into the molecular interpretation of cardiovascular diseases such as ischemic reperfusion injury.

Keywords: SNHG1; apoptosis; Hypoxia/Re-oxygenation injury;miR-21-5p; miR-30a-5p; Cardiovascular diseases