ArticleInternational ophthalmology2025
Emodin alleviates the damage to lens epithelial cells in diabetic cataract by repressing the p53-mediated ferroptosis pathway.
Article in International ophthalmology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- LPCAT3 as a Potential Drug Target for Ultraviolet Radiation-Induced Cataract: Insights From Multiomics Analysis.The Kaohsiung journal of medical sciences · 2026Article
- Lens aging and disease: Molecular mechanisms, functional consequences, and pharmacological implications.Progress in retinal and eye research · 2026Review
- Screening of natural compounds library for protection against endoplasmic reticulum stress in corneal endothelial cells.Frontiers in ophthalmology · 2026Article
- Redefining cell death: ferroptosis as a game-changer in ophthalmology.Frontiers in immunology · 2025Review
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4 authors.
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Abstract
backgroundDiabetic cataract (DC) is an ocular complication caused by diabetes. Currently, the main treatments for DC include pharmacological therapy and surgical intervention. The core objective of this study is to elucidate the specific mechanism of action of emodin in the treatment of DC, thereby providing potential targets for the treatment of DC.
methodsCCK-8 kit was used to detect the effect of emodin on the activity of lens epithelial cells (LECs). The impact of emodin on the expression of inflammatory factors and apoptosis in high glucose-induced LECs were evaluated by utilizing ELISA and flow cytometry. Then, commercial kits were performed to detect the regulatory effects of emodin on oxidative stress and ferroptosis in high glucose LECs. The potential mechanism of emodin in combating DC by inhibiting ferroptosis was analyzed by network pharmacology methods, and protein binding activity to emodin was measured by molecular docking. Besides, western blot (WB) assay was used to detect the effect of emodin on p53.
resultsFirstly, the results of CCK-8 showed that emodin could effectively alleviate the decrease of LECs cell activity and Lactate dehydrogenase (LDH) release induced by high glucose. Emodin suppressed high glucose-induced apoptosis of LECs, reduced the release of inflammatory factors, and alleviated oxidative stress and ferroptosis. GO and KEGG analyses confirmed the involvement of oxidative stress (OS), inflammatory response, and ferroptosis in the process of emodin treatment for DC. Molecular docking studies showed that emodin stably bound to proteins such as TP53, TNF, IL-6, and IL-1β. Additionally, WB results indicated that emodin alleviated high glucose-induced ferroptosis by binding to p53.
conclusionCollectively, these data suggest that emodin alleviates damage to LECs by interfering with the p53-mediated ferroptosis pathway, thereby attenuating DC disease, which offered new directions for the development of new drugs.
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