Triamcinolone Blocks Hypoxia-induced Neuronal and Inducible Nitric Oxide Synthases in Rat Retinas of Oxygen-induced Retinopathy

Ji-Myong Yoo

Purpose: Nitric oxide synthases(NOSs) are known to contribute in progression of hypoxia-induced retinal damage. In the present study, we investigated expression and changes of neuronal nitric oxide synthase(nNOS) and inducible nitric oxide synthase(iNOS) in retinas of a rat model of oxygen-induced retinopathy, and TA effect of these changes.

Materials and Methods: OIR was stimulated by exposing Sprague-Dawley (SD) rats to hyperoxia (approximately 80% O2) from postnatal day (P) 2 to P14 and then returning them to normoxia (room air, approximately 20% O2). Control rats were maintained in normoxic condition. At P15, 2μl TA solution (40 mg/ml saline) was injected into the right vitreous of rats, under an operating microscope, and saline was introduced into the left vitreous as control. All rats were sacrificed at P18. To investigate expressions of nNOS and iNOS proteins in the retinas, we performed western blot analysis, immunohistochemistry, and changes of these proteins after TA treatment are confirmed.

Results: In P18 OIR rats, proteins expressions and immunoreactivities of nNOS and iNOS proteins were significantly increased in retinas compared with controls. Immunoreacitivities of nNOS and iNOS were specific on parvalbumin-positive amacrine cells and glial fibrillary acidic protein(GFAP)-positive signals in the inner retinas, respectively. However, TA treatment effectively prevented the increases of nNOS and iNOS in retinas of P18 OIR rats.

Conclusion: Our results suggest that expression of nNOS and iNOS responded to hypoxia in the inner retina increase and TA prevents these changes.