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2000
Volume 33, Issue 1
  • ISSN: 0929-8673
  • E-ISSN: 1875-533X

Abstract

Introduction

Diabetic Retinopathy (DR) is a common microvascular issue caused by diabetes. Idebenone (IDE) is a coenzyme Q10 analog and antioxidant that has been utilized in the treatment of neurodegenerative diseases.

Methods

Our goal was to investigate how IDE might treat diabetic retinopathy. An DR model was established by injecting a single dose of streptozotocin (STZ). Rats were treated with IDE, and their vascular function was measured by ultrasound. The retina structure was checked by haematoxylin and eosin (HE) staining. The expression of biomarkers of autophagy and apoptosis was measured by Western blotting assay. The retina endothelial cell line RF/6A was stimulated with high glucose (HG) and treated with IDE. Cell proliferation and apoptosis were assessed using the Edu assay, TUNEL assay, and flow cytometry, respectively.

Results

Reduced peak systolic velocity (PSV), mean velocity (MV), end-diastolic velocity (EDV), and increased pulsatility index (PI) and resistance index (RI) were observed in diabetic rats; however, these traits were reversed by IDE therapy. IDE alleviated the STZ-induced disordered retina structure. The IDE administration suppressed DR-induced apoptosis and autophagy both and . IDE suppressed the activation of Phosphatidylinositol 3 kinase (PI3K) signaling. Activation of PI3K abolished the IDE-alleviated retina damage and cell death.

Conclusion

IDE regulated the autophagy of retina cells to alleviate diabetic retinopathy regulating the PI3K signaling pathway.

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2025-12-31
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  • Article Type:
    Research Article
Keyword(s): Diabetes; apoptosis; microvascular; muller; PI3 phosphatidylinositol 3 kinase K; retinopathy
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