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Updated: Jun 14, 2026
Oxygen-Induced Retinopathy Model for Ischemic Retinal Diseases in Rodents
Published on: September 16, 2020
Retinal protective effects of resveratrol via modulation of nitric oxide synthase on oxygen-induced retinopathy
1Department of Pediatrics, Catholic University of Daegu School of Medicine, Daegu, Korea.
Insights
Resveratrol protects against retinopathy of prematurity (ROP) by modulating nitric oxide (NO) pathways. This study shows resveratrol reduces harmful iNOS expression and increases protective eNOS and nNOS in ROP models.
Area of Science:
- Ophthalmology
- Neonatology
- Pharmacology
Background:
- Retinopathy of prematurity (ROP) is a leading cause of blindness in preterm infants.
- Increased survival rates in neonates have led to a rise in ROP incidence.
- Oxygen toxicity contributes to retinal detachment in ROP.
Purpose of the Study:
- To investigate the protective effects of resveratrol in animal and cell models of ROP.
- To determine if resveratrol modulates nitric oxide (NO) pathways in ROP.
- To analyze the expression of inducible nitric oxide synthase (iNOS), endothelial NOS (eNOS), and neuronal NOS (nNOS) in response to resveratrol.
Main Methods:
- An in vivo oxygen-induced retinopathy (OIR) model was established in Sprague-Dawley rats.
- Resveratrol was administered intravitreally in the OIR model.
- In vitro OIR was induced in primary retinal cell cultures.
- Western blotting and real-time PCR were used to assess NOS expression.
Main Results:
- Resveratrol treatment increased iNOS expression in both in vivo and in vitro OIR models.
- Resveratrol treatment decreased eNOS and nNOS expression in both OIR models.
- These changes suggest a modulation of NO-mediated mechanisms by resveratrol.
Conclusions:
- Resveratrol demonstrates retinal protective effects in OIR models.
- The protective mechanism involves the modulation of NO pathways.
- Further research into resveratrol's therapeutic potential for ROP is warranted.
Purpose:
Retinopathy of prematurity (ROP) is one of the leading causes of blindness, with retinal detachment occurring due to oxygen toxicity in preterm infants. Recently, advances in neonatal care have led to improved survival rates for preterm infants, and ROP has increased in incidence. In the present study, we aimed to determine whether or not resveratrol exhibits protective effects in an animal model of ROP and in primary retinal cell cultures of neonatal rat via nitric oxide (NO)-modulating actions using western blotting and real-time PCR with inducible nitric oxide synthase (iNOS), endothelial NOS (eNOS) and neuronal NOS (nNOS) antibodies and mRNAs.
Methods:
In an in vivo oxygen-induced retinopathy (OIR) model, cyclic hyperoxia was induced with 80% O(2) for one day and 21% O(2) for one day from P1 to P14 in newborn Sprague-Dawley (SD) rats. Resveratrol was injected intravitreally for seven days and rats were sacrificed at P21. In vitro OIR primary retinal cell culture was performed using P0-2 SD rats. Hyperoxia injuries were induced through 100% O(2) exposure for six hours. Western blotting and real-time PCR using iNOS, eNOS, nNOS antibodies and primers were performed in the rat model of ROP and the dispersed retinal cell culture.
Results:
In both in vivo and in vitro OIR, the expression of iNOS antibody and mRNA was increased and of eNOS and nNOS were reduced in the resveratrol-treated group.
Conclusions:
In conclusion, resveratrol appeared to exert retinal protective effects via modulation of NO-mediated mechanism in in vivo and in vitro OIR models.
