Third, the investigation of the interaction between apelin and VEGF did not involve the molecular signaling level. The left eye of the first monkey was used as normal control. Immunohistochemistry and reverse-transcription PCR was used to examine the expression of apelin and VEGF. The penetration of bevacizumab into the retina and iris was investigated by fluorescence immunostaining. Results Immunoreactivity for bevacizumab could be detected in the vessel walls of the iris and choroid on day 28 after injecting IVB: apelin and VEGF staining had been more prominent than normal in the CRVO eye, but these decreased following IVB injection. Expression of apelin mRNA (p 0.01) was lower in the IVB group than the CRVO group CD235 and did not vary significantly between groups. Conclusions Bevacizumab could be detected in the iris and choroid after four weeks of intravitreal injection. Apelin may be partially suppressed by bevacizumab, and it may play a role in retinal neovascularization during the development of CRVO. Introduction Central retinal vein occlusion (CRVO) is one of the most common retinal vascular diseases involving blindness . Macular edema, caused by a decline in the bloodCretina barrier, contributes to central vision loss. The decreased tissue perfusion leads to possible neovascular complications, such as rubeosis iridis and neovascular glaucoma, which can severely influence quality of life [2,3]. At present, photocoagulation has been widely used in CRVO to prevent CD235 neovascular complications. However, it cannot improve vision prognosis. Some evidence suggests that repeated intravitreal injections of triamcinolone may improve vision, but the complication of intraocular pressure and cataract makes it a less than ideal treatment . The pathogenesis of CRVO is not very well understood and remains controversial. However, it is widely accepted that vascular endothelial growth factor (VEGF) plays an important role in CRVO development . Anti-VEGF therapy, including intravitreal bevacizumab (IVB), has proven to be effective in improving visual acuity and inhibiting neovascularization [6,7]. However, research has revealed that anti-VEGF alone cannot completely prevent the occurrence of new vessels, which indicates Casp-8 that other factors may also participate in the process of neovascularization apart from VEGF . Apelin is reported to act as an angiogenic factor that could stimulate the proliferation and migration of retinal endothelial cells and vascular tube formation [9,10]. That function cannot be replaced by VEGF . Besides, recent studies suggest that apelin may be involved in retinal neovascularization during the development of proliferative diabetic retinopathy . In an eye with CRVO, hypoperfusion causes stasis of the retinal bloodstream and retinal tissue hypoxia, which might induce upregulation of apelin, simulating neovascularization thereby. To evaluate the aftereffect of apelin within the pathogenesis of CRVO, we executed the present research to look at whether bevacizumab could possibly be detected a month after IVB also to check out the appearance of apelin in eye with central retinal vein occlusion and the result of bevacizumab. Strategies Establishment of CRVO model We set up the CRVO model by obstructing all main retinal branch blood CD235 vessels (usually 2-3 blood vessels) of one eye in six rhesus monkeys. All analysis involving pets conformed to the rules from the Association for Analysis in Eyesight and Ophthalmology’s Quality Statement for the usage of Pets in Ophthalmic and Eyesight Analysis. The veins had been obstructed totally and completely by mean of the green argon laser beam (Novus Omni program; Coherent Lambda Physik, Dieburg, Germany) with energy of 400C500?mW. One of the six eye, five eye received another laser beam photocoagulation. Grouping of pets Pets had been numbered No. 1 to No. 6 and split into different groupings, as proven in Desk 1. The still left eyes of No. 1 was utilized as the regular control. The.