Current eye research · 2010
Treatment with triamcinolone acetonide prevents decreased retinal levels of decorin in a rat model of oxygen-induced retinopathy.
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Park Yeon-Jeong, Kim Young-Hee, Choi Wan-Sung, Chung In-Young, Yoo Ji-Myong
Аннотация
PURPOSE: To investigate the effect of triamcinolone acetonide (TA) on retinal expression of decorin in a rat model of oxygen-induced retinopathy (OIR).
MATERIALS AND METHODS: OIR was stimulated by exposing Sprague-Dawley (SD) rats to hyperoxia (80 +/- 1.3% O2) from postnatal day (P) 2 to P14 and then returning them to normoxia (room air, 21 +/- 1.5% O2). Control rats were maintained in normoxia. At P15, TA (40 mg/ml) was injected into the right vitreous of OIR rats and saline into the left vitreous of control rats. All rats were sacrificed at P18. RT-PCR, western blot and immunohistochemistry, TUNEL assay were performed to detect the effects of TA on molecular and morphological changes in retinal decorin levels in P18 OIR rats.
RESULTS: In P18 OIR rats, mRNA and protein of retinal levels and immunoreactivity of retinal decorin were significantly less (p-value = 0.0000000012, 0.0007, 0.000003; n = 5; respectively) than in control rats. In addition, neuronal cell death was increased in P18 OIR rats (p-value = 0.0028; n = 5) relative to controls. However, treatment with TA prevented the decrease of mRNA, protein levels, and immunoreactivity in retinal decorin in P18 OIR rats (p-value = 0.00023, 0.003, 0.000079; n = 5, respectively), and restored neuronal cell death in P18 OIR rats (p-value = 0.0022, n = 5).
CONCLUSION: Our results suggest that decorin is involved in hypoxic retinal damage and that TA protects retinal neurons damaged by relative hypoxia from decreased decorin levels.
MATERIALS AND METHODS: OIR was stimulated by exposing Sprague-Dawley (SD) rats to hyperoxia (80 +/- 1.3% O2) from postnatal day (P) 2 to P14 and then returning them to normoxia (room air, 21 +/- 1.5% O2). Control rats were maintained in normoxia. At P15, TA (40 mg/ml) was injected into the right vitreous of OIR rats and saline into the left vitreous of control rats. All rats were sacrificed at P18. RT-PCR, western blot and immunohistochemistry, TUNEL assay were performed to detect the effects of TA on molecular and morphological changes in retinal decorin levels in P18 OIR rats.
RESULTS: In P18 OIR rats, mRNA and protein of retinal levels and immunoreactivity of retinal decorin were significantly less (p-value = 0.0000000012, 0.0007, 0.000003; n = 5; respectively) than in control rats. In addition, neuronal cell death was increased in P18 OIR rats (p-value = 0.0028; n = 5) relative to controls. However, treatment with TA prevented the decrease of mRNA, protein levels, and immunoreactivity in retinal decorin in P18 OIR rats (p-value = 0.00023, 0.003, 0.000079; n = 5, respectively), and restored neuronal cell death in P18 OIR rats (p-value = 0.0022, n = 5).
CONCLUSION: Our results suggest that decorin is involved in hypoxic retinal damage and that TA protects retinal neurons damaged by relative hypoxia from decreased decorin levels.
Предметные рубрики MeSH
AnimalsAnimals, NewbornBlotting, WesternCell DeathDecorinDisease Models, AnimalExtracellular Matrix ProteinsFemaleGlucocorticoidsHumansHyperoxiaImmunohistochemistryIn Situ Nick-End LabelingInfant, NewbornOxygenPregnancyProteoglycansRNA, MessengerRatsRats, Sprague-DawleyRetinaRetinal Ganglion CellsRetinopathy of PrematurityReverse Transcriptase Polymerase Chain ReactionTriamcinolone Acetonide