Also known as choroidal noevascularization is called sub-retinal neovascularization. The essence of it is the growth of choroidal noevascularization through Bruch's membrane into the retinal pigment epithelium or under the neural retina.There are many kinds of ocular region diseases which related with choroidal noevascularization,such as age elated macular degeneration (AMD), idiopathic chorioretinitis, ocular histoplasmosis, angioid streak of eyeground, high myopia, eye contusion associated with choroidal laceration, laser photocoagulation of eyeground and so on. The permeability of vessel wall of CNV is higher than the normal blood vessel. It can easily cause to recurrent hemorrhage, exudation, cicatrization, often involving the macular area.The pathogenesis of CNV is unclear and is still not special effective method of treatment.









  At present, the purpose of all treatments are destroying CNV to terminate exudation. Treatment of new vessels inhibitive factor need to find more effective ways.The research of inhibiting angiogenesis drugs bring some hopes for the prevention of choroidal neovascularization and relapse. But the administration route, dosage, side effects and other clinical application specific details still need to do a lot of researches. The treatment goal of CNV is to recovery photoceptor、the normal anatomic relationships between the pigment epithelium and Bruch's membrane.The main hope of the future success treatment of CNV lies in the application of new anti-vascular growth factor and gene therapy. Finding effective therapy for inhibiting angiogenesis and etiopathogenisis of CNVprovid a chance for curing CNV related diseases fundamentally.









  Vasostatin is a kind of angiogenesis inhibitor which was cleaning up from supernatant of-VDS-O in B cell line from EB viral transformation by Pike,et al [7] in 1998. It was confirmed as N’structural domain of a human multifunctional protein calreculin, and 180 amino acids long. It can inhibit endothelial cells proliferation, angiogenesis and tumor growth[8]. According to reports, vasostatin in vivo and vitro showed a good inhibitive angiogenesis effect.The experiment of endothelial cells proliferation and immigration reflect the inhibition of vasostatin on endothelial cells proliferation and immigration in tumor vessel. Vasostatin inhibited neovascularization through promoting apoptosis of immature endothelial cells in new vessels and causing freshmen vascular degradation.









  The purpose of this study is to investigate the inhibition of recombinant human new vessels inhibitive factor Vasostatin on choroidal neovascularization of Nd : YAG laser-induced rats.









  Nd:YAG laser photocoagulation was performed on C57BL/6J mice to induce CNV. The 30 mice were randomly divided into three groups:control group、low-dose group and high-dose group. In treatment group , 20 ug (low-dose group ) and 40 ug (high-dose group) vasostatin were injected retrobulbarly after photocoagulation. In control group, 10ul Sodium Chloride was injected retrobulbarly. Choroidal neovascularization was evaluated on the 7th and 14th day after photocoagulation by fundus fluorescence angiography. The mice were killed on the 14th day after photocoagulation, the lesions were evaluated histologically and immunohistochemically, and the expression of CD105 was detected.The histological blades of all groups inputed imageanalytical system with 10 times object glass. In double-blind situation,we draw up the CNV membrane’s scope with the computer mouse and select the satisfied region ,then input the computer. We mark off retina- choroid region in laser light spot and determine total area and the express of masculine with HPIAS(High Resolution Pathological Image Analysis System)-1000. For the same laser spot,the largest area in consecutive sections is considered as the area of CNV ,unitsμm2.









  The FFA results of photo-coagulation C57BL/6J rats displayed the photo-coagulation position appear hyperfluorescence in artery nonage and fluorescein strengthen in anaphase opacification. The incidence of CNV was 68±16.87% in group A, 56±12.65% in group B, 48±13.98% in group C after 7 days. There was significant difference of the incidence of CNV in different groups with Kruskal-Wallis H test(P=0.021,P〈0.05). The incidence of CNV was 72±16.87% in group A, 50±14.14% in group B, 38±14.76% in group C after 14 days. There was significant difference of the incidence of CNV in different groups with Kruskal-Wallis H test(P=0.007,P〈0.01).Compared with photo-coagulation after 7 days,there are new fluorescence leakages in two photo-coagulation spot in the group A. The scope of fluorescence leakage didn’t decrease and even increased. The scope of fluorescence leakage in group B decreased and fluorescence leakage of three photo-coagulation spot disappeared. The scope of fluorescence leakage in group C decreased and fluorescence leakage of five photo-coagulation spot disappeared. The CNV lesions were smaller in vasostatin injected eyes in a dose-dependent manner.There is significant difference in it.The express of CD105 in treatment is less than the control group.









  This experiment confirmed recombinant human new vessels inhibitive factor vasostatin can increase CNV formation,but cann’t prevent CNV formation.The result prompt vasostatin has the latent value to decrease even eliminate CNV relapse as an angiogenesis inhibitor.This research induce CNV model of mice successfully through Nd:YAGlaser exposure. The way of building CNV mode provid experiment reference for pathogenesy and treatment of CNV.