Abstract

To investigate the mechanism of sodium tanshinone IIA sulfonate inhibiting hypoxia induced retinal neovascularization in rats. Forty 7 d old clean grade C57BL/6J male neonatal rats were randomly divided into control group, model group, low-dose group and high-dose group. The control group was kept in normal air for 10 d. Oxygen-induced retinopathy was studied in the model group, low-dose group, and high-dose group 30 mg/kg sodium tanshinone IIA sulfonate. The body weight of mice in all groups was measured on the 12^th and 17^th d after birth, and the area without perfusion around the optic disc was observed and calculated. The number of neovascular endothelial cells was calculated using hematoxylin and eosin staining. The expression of vascular endothelial growth factor, vascular endothelial growth factor-2 and hypoxia-inducible factor-1 were detected by Western blot. The no perfusion area around the optic disc in the model group was raised than that in the control group, and the no perfusion area around the optic disc in the low-dose group, and high-dose group was reduced than that in the model group (p<0.01). In the model group, the inner limiting membrane of retina was proliferated and disordered, and the surface was not smooth; in low-dose group, smooth limiting membrane of the retina, and a small number of endothelial cells could be seen breaking through the limiting membrane; in the high-dose group, the limiting membrane of retina was relatively complete and smooth, and the tissue structure of each layer could be seen. The number of neovascular endothelial cells in the model group was raised than that in the control group, and the number of neovascular endothelial cells in the lowdose group, and high-dose group was reduced than that in the model group, as the dose increased, it decreased (p<0.01). Vascular endothelial growth factor, vascular endothelial growth factor-2 and hypoxia-inducible factor-1 in low-dose group, and high-dose group were raised than those in control group, and those proteins expression level of in model group was reduced than control group, as the dose increased, it decreased (p<0.05). Sodium tanshinone IIA sulfonate can inhibit hypoxia induced retinal neovascularization in a dose-dependent manner, and its mechanism may be related to the regulation of vascular endothelial growth factor pathway related proteins by sodium tanshinone IIA sulfonate.