Apigenin inhibits laser-induced choroidal neovascularization and regulates endothelial cell function

The aim of this study is to evaluate the effect of apigenin on laser-induced experimental choroidal neovascularization (CNV) rat model and endothelial cell proliferation and migration.

Male Brown Norway rats were anesthetized to receive Nd:YAG laser to break the Bruch's membrane. Apigenin at 5, 15, or 30 mg/kg was given once-daily through intraperitoneal injection after laser treatment for 4 weeks. The development of CNV was determined by fluorescein angiography performed on weeks 2 and 4. Endothelial cell function was evaluated with proliferation assay and migration assay.

The intensity of fluorescein leakage from the photocoagulated lesions decreased significantly, compared to the control group, following apigenin treatment. Four (4) weeks after administration, apigenin, at 15 and 30 mg/kg, inhibited CNV development to 84.5% and 83.6% of the control group, respectively (P<0.05). Apigenin also interfered with the endothelial cells' proliferation and migration. At 3 and 10 microg/ml, apigenin inhibited the growth of human umbilical vein endothelial cells (HUVEC) to 54% and 46% of the control group, respectively (P<0.01); inhibited the growth of choroidal endothelial cells to 47% and 8% of the control group, respectively (P<0.01); and inhibited HUVEC migration over 50%, compared with the control (P<0.01).

Apigenin exerts an inhibitory effect on choroidal angiogenesis in vitro and in vivo. It should be further evaluated for its potential as a novel therapy for CNV.