To investigate the effect of octreotide acetate on neovascularization, retinal structures, and apoptotic cell death in an oxygen-induced retinopathy (OIR) mouse model. Materials and methods: A total of 26 C57BL/6J mice were exposed to 75 ± 2% oxygen from postnatal day 7 to 12. On day 12, 12 mice (group C) were injected with 0.1 µg intravitreal octreotide acetate (IVOA) and 14 mice (group D) were injected with 0.05 µg IVOA, in the right eye. The contralateral eyes were injected with 1 µL isotonic saline (control group, group B). Four mice were used as negative controls (group A). Neovascularization was quantified by counting the number of retinal vascular endothelial cell nuclei anterior to the inner limiting membrane. Structural changes were examined by light and electron microscopy. Apoptosis was investigated using the TUNEL technique. Results: The retinal vascular endothelial cell nuclei count was lower in groups C (P < 0.0001) and D (P < 0.0001) compared with group B. Light microscopy showed no retinal toxicity. Electron microscopy showed mitochondrial damage in the inner segment of the photoreceptors in the OIR mouse model without increasing in the IVOA-injected groups. There was no significant difference in the apoptotic cell death in any of the groups. Conclusion: There was mitochondrial damage in the inner segment of the photoreceptors in the OIR mouse model without increasing the apoptotic cell death.

To investigate the effect of octreotide acetate on neovascularization, retinal structures, and apoptotic cell death in an oxygen-induced retinopathy (OIR) mouse model. Materials and methods: A total of 26 C57BL/6J mice were exposed to 75 ± 2% oxygen from postnatal day 7 to 12. On day 12, 12 mice (group C) were injected with 0.1 µg intravitreal octreotide acetate (IVOA) and 14 mice (group D) were injected with 0.05 µg IVOA, in the right eye. The contralateral eyes were injected with 1 µL isotonic saline (control group, group B). Four mice were used as negative controls (group A). Neovascularization was quantified by counting the number of retinal vascular endothelial cell nuclei anterior to the inner limiting membrane. Structural changes were examined by light and electron microscopy. Apoptosis was investigated using the TUNEL technique. Results: The retinal vascular endothelial cell nuclei count was lower in groups C (P < 0.0001) and D (P < 0.0001) compared with group B. Light microscopy showed no retinal toxicity. Electron microscopy showed mitochondrial damage in the inner segment of the photoreceptors in the OIR mouse model without increasing in the IVOA-injected groups. There was no significant difference in the apoptotic cell death in any of the groups. Conclusion: There was mitochondrial damage in the inner segment of the photoreceptors in the OIR mouse model without increasing the apoptotic cell death.