ArticlePloS one2026
Dioscin attenuates D‑galactose‑induced retinal pigment epithelium senescence and epithelial-mesenchymal transition via the TGF‑β2/PI3K/Akt/β‑catenin pathway.
Article in PloS one, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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8 authors.
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Abstract
purposeThis study aimed to evaluate the protective effects of Dioscin in an age-related macular degeneration (AMD) -like model and to explore its potential therapeutic mechanisms.
methodsThe therapeutic potential of Dioscin for AMD was investigated using D-galactose-induced senescence models in ARPE-19 cells (an in vitro preliminary screening model) and C57BL/6J mice using RT-qPCR, western blotting, immunofluorescence, and SA-β-gal staining. Bioinformatic analysis and molecular docking identified TGF-β2 as a computationally predicted potential target of Dioscin in AMD. Key mechanisms involving TGF-β2 and the PI3K/Akt/β-catenin signaling pathway were assessed in vitro using RT-qPCR, western blotting.
resultsIn D-galactose-induced senescence models, Dioscin significantly alleviated RPE senescence and EMT. Single-cell transcriptome analysis revealed that TGF-β2 is highly expressed in choroidal vascular endothelial cells of AMD patients. Mechanistically, computational predictions (molecular docking and dynamics simulations) identified TGF-β2 as a computationally predicted potential target of Dioscin, and experimental data showed that Dioscin suppressed D-galactose-induced activation of the TGF-β2/PI3K/Akt/β-catenin pathway in RPE cells, suggesting a potential paracrine regulatory mechanism.
conclusionDioscin alleviates RPE senescence and EMT through suppression of the TGF-β2/PI3K/Akt/β-catenin pathway. Single-cell transcriptomics reveals that TGF-β2 is specifically upregulated in choroidal vascular endothelial cells in AMD, suggesting a paracrine mechanism linking vascular pathology to RPE dysfunction. These findings suggest that Dioscin may have potential value in mitigating RPE senescence and EMT in an AMD‑like model, although further validation in more clinically relevant AMD models is required.
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