Related Experiment Video
Updated: Sep 3, 2025
Oxygen-Induced Retinopathy Model for Ischemic Retinal Diseases in Rodents
Published on: September 16, 2020
MitoTEMPOL Inhibits ROS-Induced Retinal Vascularization Pattern by Modulating Autophagy and Apoptosis in Rat-Injected
Rova Virgana1,2, Nur Atik3, Julia Windi Gunadi4
1Department of Ophthalmology, Faculty of Medicine, Universitas Padjadjaran, Professor Eyckman 38, Bandung 40161, Indonesia.
Abstract:
Diabetic retinopathy leads to retinal malfunction, blindness, and reduced quality of life in adult diabetes patients. The involvement of reactive oxygen species (ROS) regulation stimulated by high blood glucose levels opens the opportunity for ROS modulator agents such as MitoTEMPOL. This study aims to explore the effect of MitoTEMPOL on ROS balance that may be correlated with retinal vascularization pattern, autophagy, and apoptosis in a streptozotocin-induced rat model. Four groups of male Wistar rats (i.e., control, TEMPOL (100 mg/kg body weight [BW]), diabetic (streptozotocin, 50 mg/kg BW single dose), and diabetic + TEMPOL; n = 5 for each group) were used in the study. MitoTEMPOL was given for 5 weeks, followed by funduscopy, and gene and protein expression were explored from the rat's retina. Streptozotocin injection decreased bodyweight and increased food and water intake, as well as fasting blood glucose. The results showed that MitoTEMPOL reduced retinal vascularization pattern and decreased superoxide dismutase gene expression and protein carbonyl, caspase 3, and caspase 9 protein levels. A modulation of autophagy in diabetes that was reversed in the diabetic + TEMPOL group was found. In conclusion, MitoTEMPOL modulation on autophagy and apoptosis contributes to its role as a potent antioxidant to prevent diabetic retinopathy by inhibiting ROS-induced retinal vascularization patterns.
Insights
MitoTEMPOL, a reactive oxygen species (ROS) modulator, shows promise in preventing diabetic retinopathy by inhibiting ROS-induced retinal vascularization and regulating autophagy and apoptosis in diabetic rats.
Area of Science:
- Biomedical Science
- Ophthalmology
- Endocrinology
Background:
- Diabetic retinopathy (DR) is a leading cause of blindness in adults with diabetes, characterized by retinal malfunction.
- High blood glucose levels in diabetes elevate reactive oxygen species (ROS), contributing to DR pathogenesis.
- ROS modulators, like MitoTEMPOL, present a potential therapeutic strategy for DR.
Purpose of the Study:
- To investigate the effects of MitoTEMPOL on ROS balance in a rat model of diabetic retinopathy.
- To explore the correlation between MitoTEMPOL treatment, retinal vascularization, autophagy, and apoptosis in diabetic rats.
Main Methods:
- A streptozotocin-induced diabetic rat model was used, with four experimental groups: control, TEMPOL, diabetic, and diabetic + TEMPOL.
- Rats were treated with MitoTEMPOL for five weeks.
- Retinal vascularization, gene expression (superoxide dismutase), and protein levels (caspase 3, 9, protein carbonyl) were analyzed.
Main Results:
- MitoTEMPOL treatment reduced retinal vascularization and decreased markers of oxidative stress and apoptosis (superoxide dismutase, protein carbonyl, caspase 3, and caspase 9).
- Diabetic rats exhibited altered autophagy, which was reversed by MitoTEMPOL treatment.
- MitoTEMPOL modulated autophagy and apoptosis in the diabetic rat retina.
Conclusions:
- MitoTEMPOL acts as a potent antioxidant, inhibiting ROS-induced retinal vascularization patterns in diabetic retinopathy.
- MitoTEMPOL's modulation of autophagy and apoptosis contributes to its protective effects against diabetic retinopathy.
- This study supports MitoTEMPOL as a potential therapeutic agent for preventing diabetic retinopathy.
