M echanism of lncRNA FOXD3 AS1 targeting miR 338 3p in human lens epithelial cell injury in diabetic cataract
نویسندگان
چکیده
Purpose: To explore the influence of lncRNA FOXD3-AS1 on high glucose (HG)-stimulated human lens epithelial cell injury in diabetic cataract. Methods: Lens HLEB3 were cultured vitro and transfected with si-FOXD3-AS1, miR-338-3p mimic or inhibitor, followed by HG (40 mmol/L) treatment. FOXD3-AS1, miR-338-3p, cleaved caspases3 caspases9 expression analyzed RT-qPCR western blot. SOD CAT activities MDA production cells determined using special kits. Cell apoptotic rate was quantified flow cytometry. Regulatory relationship investigated mechanism assay. Results: enhanced but repressed (P<0.05) cells. FoxD3-AS1 depletion introduction promoted activities, decreased content, apoptosis rate, protein HG-induced (P<0.05). could target negatively regulate miR-338-3p. FOXD3-AS1-mediated rescued inhibitors. Conclusion: silenced upregulated to alleviate oxidative stress
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ژورنال
عنوان ژورنال: Tropical Journal of Pharmaceutical Research
سال: 2023
ISSN: ['1596-5996', '1596-9827']
DOI: https://doi.org/10.4314/tjpr.v22i3.10