ArticleMolecular biology reports2025
Ginkgo Biloba extract attenuates diabetic retinopathy progression by modulating TP53 ubiquitination in a rat model.
Article in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Effects of Ginkgo biloba extract on glycemic control, inflammatory markers, lipid profile, anthropometric indices, and safety parameters in patients with metabolic syndrome and type 2 diabetes: a meta-analysis.Diabetology & metabolic syndrome · 2026Review
- Berberine alleviates pyroptosis of retinal ganglion cells in diabetic retinopathy by regulating AKT1, JUN, and STAT3.Ibrain · 2026Article
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2 authors.
Funding
Abstract
backgroundDiabetic retinopathy (DR) is a microvascular complication of diabetes characterized by damage to the retina's neurons and blood vessels. Ginkgo biloba extract (GBE) has demonstrated neuroprotective properties, however, its specific mechanisms in DR remain incompletely understood. This research aims to elucidate the underlying mechanisms of GBE in DR. METHODS AND
resultsA diabetic rat model was induced with streptozotocin (STZ) and divided into control, diabetic, and GBE-treated groups. Retinal tissues of each group were analyzed using histology, TUNEL staining, and immunofluorescence. Bioinformatics identified potential GBE targets for DR, and protein-protein interaction network analysis prioritized core targets. Western blot and immunoprecipitation assays were used to detect protein expression and ubiquitination status. We successfully constructed the DR rat models and observed that GBE intervention effectively reverses diabetes-induced hyperglycemia and mitigates retinal ganglion cell (RGC) damage in the DR rat model. TUNEL staining indicates GBE's protective role against RGC apoptosis induced by DR. Bioinformatics identified 135 GBE targets in DR, with a focus on apoptosis pathways. Critically, we demonstrated an upregulation of TP53 expression in the retinal tissues of the DR rat model, an effect that was successfully reversed following GBE intervention. Notably, GEB increased TP53 ubiquitination, suggesting a potential modulation of TP53 stability and function.
conclusionsGBE attenuates DR progression by modulating TP53 ubiquitination in a rat model. The findings highlight the potential therapeutic benefits of GBE in DR and suggest further investigation into its mechanisms and broader bioactivity pathways.
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