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Original Research Article | OPEN ACCESS

Circ_0001953 contribute to retinal vascular endothelial cell injury induced by high glucose through regulating miR-186

Yazhen Yuan1 , Yongqing Guan1, Chenjun Shao1, Hui Wang2, Shuangmei Zhang1

1Department of Ophthalmology, the Fourth Hospital of Hebei Medical University, Shijiazhuang, Hebei Province, 050000, China; 2Department of Ophthalmology, Shijiazhuang People's Hospital, Shijiazhuang, Hebei Province, 050003, China.

For correspondence:-  Yazhen Yuan   Email: uyd3365@126.com

Accepted: 26 February 2023        Published: 31 March 2023

Citation: Yuan Y, Guan Y, Shao C, Wang H, Zhang S. Circ_0001953 contribute to retinal vascular endothelial cell injury induced by high glucose through regulating miR-186. Trop J Pharm Res 2023; 22(3):563-569 doi: 10.4314/tjpr.v22i3.13

© 2023 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 investigate the effects of circ_0001953/miR-186 on human retinal vascular endothelial cell (HRVEC) injury evoked by high glucose.  
Methods: A cell model (HG group) was established using high glucose-treated HRVECs, while untreated HRVECs were used as the control group (Con group). The levels of endothelin-1 (ET-1), ICAM-1 and IL-6 were evaluated by ELISA and the content of malondialdehyde (MDA) and superoxide dismutase (SOD) in HRVECs were determined. Apoptosis rate was tested adopting flow cytometry. The interrelationship between circ_0001953 and miR-186 was assessed using dual luciferase reporter assay. Measurement of Bax and Bcl-2 was implemented via western blot.
Results: In HG group, circ_0001953 increased while miR-186 was downregulated, ET-1, IL-6, ICAM-1, and apoptosis rate increased and accompanied with up-regulated Bax content and declined Bcl-2 protein level. Furthermore, the content of MDA increased and SOD decreased. MiR-186 was a target of circ_0001953.
Conclusion: Inhibition of circ_0001953 can repress inflammation, oxidative stress and apoptosis in HRVECs by up-regulating the expression of miR-186.

Keywords: circ_0001953, miR-186; HRVECs, inflammation; oxidative stress, apoptosis

Impact Factor
Thompson Reuters (ISI): 0.523 (2021)
H-5 index (Google Scholar): 39 (2021)

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