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Original Research Article | OPEN ACCESS

Mechanism of lncRNA FOXD3-AS1 targeting miR-338-3p in human lens epithelial cell injury in diabetic cataract

QingWei Du1, LiLun Wang2, Mei Li3

1Department of Ophthalmology, Yanan University Affiliated Hospital, Yanan, Shaanxi Province, 716000, China; 2Department of Ophthalmology, Yanan University Affiliated Hospital, Yanan, Shaanxi Province, 716000, China; 3Yan"An Peoples Hospital, 57 Qilipu Street, Baota District, Yanan City, Shaanxi Province, 716000, China.

For correspondence:-  Mei Li   Email: yub95882@126.com

Accepted: 12 March 2023        Published: 31 March 2023

Citation: Du Q, Wang L, Li M. Mechanism of lncRNA FOXD3-AS1 targeting miR-338-3p in human lens epithelial cell injury in diabetic cataract. Trop J Pharm Res 2023; 22(3):535-542 doi: 10.4314/tjpr.v22i3.10

© 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 explore the influence of lncRNA FOXD3-AS1 on high glucose (HG)-stimulated human lens epithelial cell injury in diabetic cataract.
Methods: Lens epithelial cell HLEB3 were cultured in vitro and transfected with si-FOXD3-AS1, miR-338-3p mimic or miR-338-3p inhibitor, followed by HG (40 mmol/L) treatment. FOXD3-AS1, miR-338-3p, cleaved caspases3 and cleaved caspases9 expression were analyzed by RT-qPCR or western blot. SOD and CAT activities and MDA production in cells were determined using special kits. Cell apoptotic rate was quantified by flow cytometry. Regulatory relationship of FOXD3-AS1 and miR-338-3p was investigated by mechanism assay.
Results: HG enhanced FOXD3-AS1 expression but repressed miR-338-3p (P<0.05) in HLEB3 cells. FoxD3-AS1 depletion or miR-338-3p introduction promoted SOD and CAT activities, decreased MDA content, apoptosis rate, and cleaved caspases3 and cleaved caspases9 protein production in HG-induced HLEB3 cells (P<0.05). FOXD3-AS1 could target and negatively regulate miR-338-3p. FOXD3-AS1-mediated influence on HG-induced HLEB3 cells was rescued by miR-338-3p inhibitors.
Conclusion: FOXD3-AS1 silenced upregulated miR-338-3p expression to alleviate HG-induced oxidative stress and apoptosis of HLEB3 cells.

Keywords: Apoptosis; Diabetic cataract; FOXD3-AS1; miR-338-3p; oxidative stress

Impact Factor
Thompson Reuters (ISI): 0.6 (2023)
H-5 index (Google Scholar): 49 (2023)

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