Abstract
Purpose: :
To examine whether intravitreal triamcinolone acetonide reduces apoptosis in the retina of eyes of retinopathy of prematurity (ROP) mouse model.
Methods: :
Mice (n=11) were incubated from P7–P12 with 75% O2. At P12, 1 µl of crystalline triamcinolone acetonide was injected into the vitreous of one eye. The contralateral eye served as a control. At P15 (n=5) and P17 (n=6) mice were sacrificed and eyes were analyzed (study group). As negative control, 6 mice (no ROP, no treatment) were sacrificed at P15 (control group). Using a TUNEL apoptosis assay (Promega) all positive cells were counted. Statistical analysis was performed with SPSS.
Results: :
In all examined eyes, the mean number of stained cells was significantly (p>0.05) higher in the outer nuclear retinal layer (22.01± 14.6 ) and inner nuclear retinal layer (7 ± 7.76 ) than in the other retinal layers . In all eyes examined, the number of apoptotic cells was significantly higher in the central retinal region (24 ± 16.2) than in the periphery of the retina (9 ± 8.21). The count of fluorescent cells was significantly (p<0.05) higher in the study group (17 ± 12.37) than in the control group (6 ± 5.34). In the study group, the amount of apoptotic retinal cells in the nuclear layers increased from day P15 (13 ± 11.96) to day P17 (17 ± 3.05). The study group eyes treated with triamcinolone (13 ± 11.96) compared with the contralateral, not treated eyes (13 ± 2.48), showed no statistically significant difference in the count of apoptotic retinal cells.
Conclusions: :
Induced retinal neovascularization in the retinopathy of prematurity model of the mouse results in a high number of apoptotic retinal cells. Intravitreal triamcinolone acetonide does not markedly reduce the amount of apoptosis induced by retinopathy of prematurity.
Keywords: retinal neovascularization • apoptosis/cell death • corticosteroids