Effects of epoxyeicosatrienoic acids (EETs) on retinal macular degeneration in rat models

OBJECTIVE: Here we use a rat model to investigate the effects of epoxyeicosatrienoic acids (EETs) on retinal macular degeneration along with pathological and physiological mechanisms of the disease.

MATERIALS AND METHODS: Six choroidal neovascularization (CNV) rats were created with a 532 nm laser and received intravitreal injections of EETs in both eyes. On day 1, 3, 7 and 14 after photocoagulation, the thickness and area of CNV were measured with HE staining and choroidal flat mounts. COX-2 and VEGF levels in CNV were detected by immunohistochemistry method. Protein and mRNA expression were studied by Western blotting and RT-PCR.

RESULTS: 14 days after photocoagulation, CNV thickness and area were significantly reduced (p<0.01) in the treatment group compared with the control group. COX-2 and VEGF had high expression in vascular endothelial cells and stromal cells of CNV. Peak expression of COX-2 and VEGF was significantly higher (p<0.01) in the treatment group than in the control group. 7 days after photocoagulation, VEGF protein and mRNA expression were significantly lower (p<0.05) in the treatment group than in the control group, whereas COX-2 mRNA showed no significant difference (p>0.05). FFA found that CNV fluorescein leakage area was significantly reduced (p<0.05) in the treatment group than in the control group. 14 days after photocoagulation, neovascularization area was significantly smaller (p<0.05) in the treatment group than in the control group. Vitreous EETs levels in the treatment group were significantly higher than in the control group. Compared with the control group, the celecoxib treatment group had significantly increased vitreous EETs (p<0.05).

CONCLUSIONS: Intravitreal injection of celecoxib could suppress the thickness and area of laser-induced macular degeneration CNV. It also improved the vitreous EETs levels in CNV model rats. COX-2 expression was upregulated in the early generation of laser-induced CNV, which may play an important role in regulating expression of VEGF.

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