SODIUM FERULATE INHIBITS RETINAL NEOVASCULARIZATION IN RETINOPATHY OF PREMATURITY MODEL RATS BY DOWNREGULATING VEGF EXPRESSION IN HRCECS

Objective: This study explores the inhibitory effect of sodium ferulate on retinal neovascularization in retinopathy of prematurity model rats by downregulating the expression of objective endothelial growth factor (VEGF) in humans retinal vascular endothelial cells (HRCECs). Methods: Thirty-six male C57BL / 6J pups were randomly divided into three control, model, and sodium ferulate groups (treatment group), with 12 pups (24 eyes) in each. The model of retinopathy of prematurity was established. The control group was fed in the natural air. The model and treatment groups were continuously fed in the oxygen box with their mothers. After feeding in the hyperoxia environment for one week, they were taken out and fed in the natural air. At this time, the young rats were 14 days old and continued to feed for one week. The treatment group was injected with sodium ferulate 25 mg/kg intraperitoneally. The young rats were 21 days old. Retinal blood vessels, retinal tissue, and the number of vascular endothelial cells breaking through the retinal inner limiting membrane were observed. HRCECs were cultured and divided into low glucose control, high glucose model, low-dose sodium ferulate, and high-dose sodium ferulate groups. The sodium ferulate effects on the proliferation of HRCECs and the expression of VEGF in HRCECs were detected. Results: In the control group, retinal vessels were evenly distributed and well-branched on day 14; On the 21st day, retinal vessels were basically mature. In the model group, the retinal vessels were significantly reduced, and a large number of non-perfusion areas appeared on the 14th day. On the 21st day, many new blood vessels with disordered distribution and structure appeared. The treatment group was the same as the model group on the 14th day. On day 21, the vascular density decreased significantly. In the control group, retinal cells were arranged orderly, and no or few vascular endothelial cells were breaking through the retinal inner limiting membrane. In the model group, many vascular endothelial cells broke through the inner limiting membrane of the retina and dilated blood vessels were observed. The number of vascular endothelial cells breaking through the retinal internal limiting membrane in the treatment group was significantly less than that in the model group. Compared with the low glucose control group, the proliferation ability of HRCECs in the high glucose model group was significantly enhanced, and the expression level of VEGF in HRCECs was significantly increased (P<0.05). Compared with the high glucose model group, the proliferation ability of HRCECs in the sodium feulate group was significantly decreased, and the expression level of VEGF in HRCECs was decreased considerably. With the increase in sodium ferulate dose, the proliferation ability of HRCECs was gradually weakened, and the expression level of VEGF was gradually decreased (P<0.05). Conclusion: Sodium ferulate can inhibit retinal neovascularization in mice with retinopathy of prematurity, which may be achieved by inhibiting VEGF expression in HRCECs cells.