Dioscin attenuates D‑galactose‑induced retinal pigment epithelium senescence and epithelial–mesenchymal transition via the TGF‑β2/PI3K/Akt/β‑catenin pathway
- 1The National and Local Joint Engineering Laboratory of Animal Peptide Drug Development, College of Life Sciences, Hunan Normal University, Changsha, China
- 2Engineering Research Center for Antibodies from Experimental Animals of Hunan Province, College of Life Sciences, Hunan Normal University, Changsha, China
Abstract
Purpose: This 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. Methods: The 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. Results: In 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. Conclusion: Dioscin 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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BibTeX
@article{ouyang2026dioscin,
title = {{Dioscin attenuates D‑galactose‑induced retinal pigment epithelium senescence and epithelial–mesenchymal transition via the TGF‑β2/PI3K/Akt/β‑catenin pathway}},
author = {Qi Ouyang and Huiqin Zhou and Chenhao Ji and Hong Jiang and Linhui Zhao and Yiwei Pan and Shuanglin Xiang and Xiang Hu},
journal = {PLOS One},
year = {2026},
month = sep,
doi = {10.1371/journal.pone.0359423},
url = {https://doi.org/10.1371/journal.pone.0359423},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Dioscin attenuates D‑galactose‑induced retinal pigment epithelium senescence and epithelial–mesenchymal transition via the TGF‑β2/PI3K/Akt/β‑catenin pathway
AU - Qi Ouyang
AU - Huiqin Zhou
AU - Chenhao Ji
AU - Hong Jiang
AU - Linhui Zhao
AU - Yiwei Pan
AU - Shuanglin Xiang
AU - Xiang Hu
PY - 2026
DA - 2026/09/28
JO - PLOS One
DO - 10.1371/journal.pone.0359423
UR - https://doi.org/10.1371/journal.pone.0359423
AB - Purpose: This 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. Methods: The 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. Results: In 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. Conclusion: Dioscin 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.
SN - 1932-6203
ER -