Title:Idebenone Attenuates Diabetic Retinopathy by Modulating
Autophagy via Targeting Akt Signaling
Volume: 33
Issue: 1
Author(s): Zhenqian Yu and Gang Liu*
Affiliation:
- Department of Ophthalmology, Qilu Hospital
(Qingdao), Cheeloo College of Medicine, Shandong University, 758 Hefei Road, Qingdao, Shandong,
266035, China
Keywords:
Diabetes, apoptosis, PI3 phosphatidylinositol 3 kinase K, microvascular, retinopathy, muller.
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.
Method: Our goal was to investigate how IDE might treat diabetic retinopathy. An in
vivo 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.
Result: 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 in vivo and in vitro. 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
via regulating the PI3K signaling pathway.
