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Corilagin alleviates ferroptosis in diabetic retinopathy by activating the Nrf2 signaling pathway
Wenxin Shi1, Yuchen Dong1, Shuyan Liu1
1Department of Ophthalmology, The Second Hospital of Jilin University, Changchun, China.
Background And Purpose:
Diabetic retinopathy (DR) is a prevalent complication of diabetes, with a rising global incidence, and can result in significant vision impairment and potential blindness in adults. Corilagin (COR) has been shown to regulate several pathological processes. However, the specific protective role and mechanism of action of COR in DR remain unknown.
Experimental Approach:
The protective effects and mechanisms of COR in DR were examined using the ARPE-19 cell line and C57BL/6 mice. Intraretinal tissue damage and molecular markers were evaluated to investigate the impact of COR on oxidative stress and cell death pathways.
Key Results:
In vitro, COR significantly reduced the cytotoxic effects of high glucose (HG) on ARPE-19 cells. Furthermore, COR also effectively decreased HG-induced lipid peroxidation, iron deposition, and ferroptosis and reduced damage to retinal tight junction proteins. Similarly, an in vivo study of streptozotocin (STZ)-induced DM mice showed that the daily gavage of COR for eight weeks notably alleviated DR. Mechanistically, COR activated the Nrf2 antioxidant signaling pathway both in vivo and in vitro, preventing HG-induced alterations in morphological and biochemical parameters. Notably, our study demonstrated that compared with controls, Nrf2 knockout mice and siNrf2-treated cells were more vulnerable to ferroptosis under HG conditions, and the protective effect of COR on DR was substantially diminished in these models.
Conclusion And Implications:
These data indicate that COR has a protective effect against HG-induced retinal injury via a mechanism associated with the Nrf2-dependent antioxidant pathway and ferroptosis regulation.
Insights
Corilagin (COR) protects against diabetic retinopathy (DR) by activating the Nrf2 antioxidant pathway, reducing oxidative stress and ferroptosis in retinal cells. This study elucidates COR
Area of Science:
- Ophthalmology
- Endocrinology
- Molecular Biology
Background:
- Diabetic retinopathy (DR) is a leading cause of vision loss in diabetic patients.
- The protective mechanisms of Corilagin (COR) in DR are not well understood.
- Diabetes mellitus (DM) complications necessitate novel therapeutic strategies.
Purpose of the Study:
- To investigate the protective effects of Corilagin (COR) against diabetic retinopathy (DR).
- To elucidate the underlying molecular mechanisms of COR's action in DR.
- To evaluate COR's impact on oxidative stress and cell death pathways in retinal injury.
Main Methods:
- In vitro studies using ARPE-19 cells exposed to high glucose (HG).
- In vivo studies utilizing streptozotocin (STZ)-induced diabetic mice.
- Evaluation of intraretinal tissue damage, molecular markers, oxidative stress, and ferroptosis.
- Assessment of the Nrf2 signaling pathway's role.
Main Results:
- Corilagin (COR) significantly reduced high glucose (HG)-induced cytotoxicity, lipid peroxidation, iron deposition, and ferroptosis in ARPE-19 cells.
- COR treatment in diabetic mice alleviated DR symptoms and protected retinal tight junction proteins.
- COR activated the Nrf2 antioxidant signaling pathway, mitigating HG-induced damage.
- Nrf2 knockout models showed increased vulnerability to ferroptosis and diminished COR protection.
Conclusions:
- Corilagin (COR) demonstrates significant protective effects against high glucose-induced retinal injury.
- The protective mechanism involves the Nrf2-dependent antioxidant pathway and regulation of ferroptosis.
- COR represents a potential therapeutic agent for managing diabetic retinopathy.
