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

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.