Keywords
diabetic retinopathy; gene expression profiling; glycitin; oxidative stress; premature senescence
Abstract
Diabetic retinopathy (DR) is a leading cause of vision loss, which is driven in part by oxidative stress-induced dysfunction of ocular tissues. We previously showed that high glucose conditions trigger senescence pathways and damage the retinal pigment epithelium (RPE). Here, we identify glycitin, a natural isoflavone, as a candidate cytoprotectant and define its mechanism of action in high glucose-exposed ARPE-19 cells. Using RNA-seq followed by Ingenuity Pathway Analysis, we mapped glycitin-responsive programs and validated key nodes experimentally. Glycitin partially restored cell proliferation, suppressed oxidative stress, and reversed high glucose-induced premature senescence, primarily through modulation of the PI3K/AKT pathway. These findings suggest that glycitin could be a promising modulator of RPE resilience and support its further development for preventing or treating DR and other types of retinal degeneration.
Recommended Citation
Sheu, Shwu-Jiuan; Lin, Yi-Hsiung; Lin, Ching-Yu; He, Chen-Xi; Li, Chia-Yang; Tu, Shun-Yuan; Tsai, Yi-Ching; Cheng, Kai-Chun; Chiu, Chien-Chih; and Chen, Chun-Lin
(2026)
"Glycitin Primes Retinal Pigment Epithelium Resilience to High-Glucose Injury via the PI3K/AKT Pathway,"
Journal of Food and Drug Analysis: Vol. 34
:
Iss.
4
, Article 3.
Available at: https://doi.org/10.38212/2224-6614.3610
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