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Updated: May 20, 2026
Oxygen-Induced Retinopathy Model for Ischemic Retinal Diseases in Rodents
Published on: September 16, 2020
[Anti-angiogenesis effect of AMD3100 in oxygen-induced retinopathy mice]
Qing-yue Xu1, Yuan-zhi Yuan, Li-yang Wang
1Department of Ophthalmology, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Objective:
To observe the inhibition of neovascularisation in the oxygen-induced retinopathy (OIR) mice by a stromal cell-derived factor 1 (SDF-1) antagonist.
Methods:
Experimental study. Fifty-eight 7-day-old C57BL/6 mice were divided into 3 groups randomly, the control group (n = 17), the test group (n = 17) and the medication group (n = 24). According to the dosage of AMD3100, the medication group (n = 24) were divided into low dose group, high dose group, low dose control group, and high dose control group (each group n = 6). Each group (19-day-old) was sacrificed to perform ADPase staining, paraffin sections and immunohistochemical staining (anti-VEGF and anti-SDF-1). The average positive staining area percentage (APSAP) was measured as the outcomes and processed with the Students' t-test.
Results:
Real-time PCR showed expression of both VEGF mRNA (0.080 ± 0.022 vs. 0.123 ± 0.032) and SDF-1 mRNA (0.731 ± 0.099 vs.0.544 ± 0.108) in retinas from the control group and test group, respectively. The expression of these factors in the test group was significantly higher (t = 2.488, P = 0.038;t = 2.864, P = 0.021). The number of neovascular endothelial nuclear that broke through the retinal internal limiting membrane in the paraffin section in the high dose group and the low dose group was significantly less than that in the self-control group (t = -9.507, P = 0.000; t = -10.761, P = 0.000). The appearance of ADPase staining sections in the medication group was more similar to the simple control group than that of the test group. Immunohistochemical staining sections showed that VEGF and SDF-1 expressed in neuroepithelial cells in each group. APSAP in the high dose group and the low dose group was significantly lower than that in the self-control group (VEGF: t = -7.249, P = 0.000; t = -9.02, P = 0.000; SDF-1: t = -5.246, P = 0.000; t = -5.216, P = 0.000).
Conclusion:
These results indicate that AMD3100 block the SDF-1 receptor to reduce the effect of SDF-1, decrease the production of VEGF protein and inhibite neovascularization.
Insights
AMD3100, a stromal cell-derived factor 1 (SDF-1) antagonist, effectively inhibits neovascularization in oxygen-induced retinopathy (OIR) mice. This drug reduces vascular endothelial growth factor (VEGF) production by blocking the SDF-1 receptor.
Area of Science:
- Ophthalmology
- Molecular Biology
- Pharmacology
Background:
- Neovascularization is a key pathological process in oxygen-induced retinopathy (OIR).
- Stromal cell-derived factor 1 (SDF-1) and vascular endothelial growth factor (VEGF) play critical roles in promoting neovascularization.
Purpose of the Study:
- To investigate the inhibitory effect of AMD3100, an SDF-1 antagonist, on neovascularization in a mouse model of OIR.
- To evaluate the impact of AMD3100 on VEGF and SDF-1 expression in the context of OIR.
Main Methods:
- An experimental study involving 58 C57BL/6 mice subjected to oxygen-induced retinopathy.
- Mice were randomized into control, test, and medication groups (treated with varying doses of AMD3100).
- Histopathological analyses included ADPase staining, paraffin sections, and immunohistochemical staining for VEGF and SDF-1; quantitative analysis of Average Positive Staining Area Percentage (APSAP) was performed.
Main Results:
- AMD3100 treatment significantly reduced the number of neovascular endothelial nuclei penetrating the retinal internal limiting membrane.
- Real-time PCR indicated altered VEGF and SDF-1 mRNA expression in response to OIR, with AMD3100 treatment showing significant reductions in APSAP for both VEGF and SDF-1.
- Immunohistochemical staining confirmed VEGF and SDF-1 expression in neuroepithelial cells, with AMD3100 treatment leading to significantly lower APSAP values.
Conclusions:
- AMD3100 effectively inhibits neovascularization in OIR mice.
- The mechanism involves blocking the SDF-1 receptor, leading to reduced SDF-1 effects and decreased VEGF production.
- AMD3100 demonstrates therapeutic potential for treating neovascular eye diseases.
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