Open Access

ARTICLE

Blueberry anthocyanins extract attenuates oxidative stress and angiogenesis on an in vitro high glucose-induced retinopathy model through the miR-33/GLCCI1 axis

by WENBIN LUO¹, YULING ZOU², HONGXI WU³, ZHONGYI YANG¹, ZHIPENG YOU^2,*

1 Department of Ophthalmology, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, 330000, China
2 Department of Ophthalmology in Ocular Fundus Diseases, Affiliated Eye Hospital of Nanchang University, Nanchang, 330000, China
3 Department of Ophthalmic Treatment of Refractive Errors, Affiliated Eye Hospital of Nanchang University, Nanchang, 330000, China

* Corresponding Author: ZHIPENG YOU. Email:

BIOCELL 2024, 48(8), 1275-1284. https://doi.org/10.32604/biocell.2024.051045

Received 26 February 2024; Accepted 27 May 2024; Issue published 02 August 2024

Abstract

Background: Diabetes retinopathy (DR) is a complication of diabetes that affects patients’ vision. Previous studies have found blueberry anthocyanins extract (BAE) can inhibit the progression of DR, but its mechanism is not completely clear. Methods: To study the role of BAE in diabetes retinopathy, we treated human retinal endothelial cells (HRCECs) with 30 mM high glucose to simulate the microenvironment of diabetes retinopathy and used BAE to intervene the in vitro high glucose-induced retinopathy model. HRCEC cell viability and apoptosis rates were examined by Cell Counting Kit 8 (CCK-8) assay and flow cytometry assay. The binding sites between miR-33 and glucocorticoid-induced transcript 1 (GLCCI1) were assessed by luciferase reporter assay. Retinal neovascularization and oxidative stress contribute to diabetic retinopathy. The tubule formation assay was applied to detect the retinal neovascularization. The oxidative stress in the HRCECs was manifested by the reactive oxygen species (ROS) level, the malondialdehyde (MDA) level, and the superoxide dismutase (SOD) activity. Results: Compared with HRCECs cells cultured under normal conditions, high glucose (HG) can induce oxidative stress in HRCRCs, specifically manifested in the increase of ROS and MDA levels, and the decrease of SOD activity. BAE relieved the tubule formation in n the HRCEC. BAE also relieved the ROS and MDA levels and increased the SOD activity. Luciferase reporter assay revealed that GLCCI1 is a target molecule downstream of miR-33. In HRCEC, BAE significantly inhibited the expression of miR-33 induced by HG. miR-33 mimic inhibited the BAE’s effects on oxidative stress and angiogenesis in an in vitro high glucose-induced retinopathy model. Conclusion: BAE alleviated the oxidative stress and microangiogenesis of HRCEC by regulating the miR-33 /GLCCI1 axis.

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