Figure 5. H-RN inhibits retinal neovascularization. A: Retinal vascular distribution of a normal pup raised in room air. B: This figure shows a representative retina from 17-day-old pups that were subjected to 5 days of 75% oxygen tension and then maintained in room air for an additional 5 days. Circles indicate the neovascular tufts. C: A retina from a mouse pup injected with vascular endothelial growth factor ab (VEGFab; 50 ng/µl). D: A retina from a mouse pup injected with H-RN (50 mM). E: A retina from a mouse pup injected with H-FT (50 mM). F: A retina from a mouse pup injected with scrambled peptide (50 mM, magnification, ×40). G: A hematoxylin- and eosin-stained section of P17 control raised in room air. H: P17 retina exposed to hyperoxia from P7 to P12, and returned to room air from P12 to P17. Arrows indicate neovascular tufts extending into the vitreous. I: A section from 50 ng/µl VEGFab-treated hyperoxia group. J: A section from 50 mM H-RN-treated hyperoxia group. The retina of I and J presented obvious reduced abnormal neovascularization tufts (arrows). K: A section from 50 mM H-FT-treated hyperoxia group. L: A section from 50 mM scrambled peptide treated hyperoxia group (magnification, ×400). M: Quantification of neovascular lumens response to hyperoxia. Lumens extending from the internal limiting membrane into the vitreous were counted. Data in each column present means±SD values of total number of vascular lumens per retinal cross-section, from 7 to 9 eyes of 7–9 mice. Note that the lumens in VEGFab and H-RN-treated group are reduced significantly more than the control and PBS groups (p<0.001), while the number of lumens in the H-FT and scrambled peptide-treated group had no difference from the control and PBS treated group (p>0.05). These experiments were repeated three times with similar results (** p<0.01, each condition versus control).