title: Bevacizumab inhibits corneal neovascularization in an alkali burn induced model of corneal angiogenesis.
abstract: BACKGROUND
  New and uncontrolled blood vessel development in the cornea is a pivotal process in the pathogenesis of several corneal diseases. These corneal diseases may finally cause blindness and managing them therapeutically is problematic. The data supporting a causal role for vascular endothelial growth factor in corneal neovascularization are extensive. This study aimed to evaluate the effect of subconjunctival bevacizumab (Avastin) on experimental corneal neovascularization in rabbits.
  
  
  METHODS
  Chemical cauterization of the cornea was performed by touching central cornea with a 5-mm-diameter NaOH-soaked cotton applicator for 10 s in 20 eyes of 20 White New Zealand rabbits. The rabbits were then divided randomly into two equal groups. Bevacizumab (2.5 mg) was administered to 10 eyes (group 1) by a subconjunctival injection immediately after chemical cauterization of corneal surface. As a control, 10 eyes (group 2) received an injection of distilled water. Rabbits were examined daily for detection of the first signs of neovascularization. Three weeks later, the extent of corneal neovascularization was evaluated by direct examination and photograph analyses. Total corneal neovascularization area, degree of circumference involved and longest neovascular pedicle length were assessed.
  
  
  RESULTS
  Bevacizumab significantly decreased the total neovascularization area (P < 0.009), the circumference involved (P < 0.011) and the longest neovascular pedicle length (P < 0.023).
  
  
  CONCLUSIONS
  Local injection of bevacizumab has a significant effect on inhibition of alkali burn-induced corneal neovascularization. This shows the potential value of bevacizumab in the treatment of corneal neovascularization.
authors.affiliation: Shiraz University of Medical Sciences, Department of Ophthalmology, Khalili hospital, Shiraz, Iran. hosseini.hamid@gmail.com
authors.forename: Hamid
authors.initials: H
authors.lastname: Hosseini
authors.forename: Mahmood
authors.initials: M
authors.lastname: Nejabat
authors.forename: Morsal
authors.initials: M
authors.lastname: Mehryar
authors.forename: Taher
authors.initials: T
authors.lastname: Yazdchi
authors.forename: Ahad
authors.initials: A
authors.lastname: Sedaghat
authors.forename: Farajollah
authors.initials: F
authors.lastname: Noori
mesh_terms: D020533:Angiogenesis Inhibitors / Q000627:therapeutic use*; D000818:Animals; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D061067:Antibodies, Monoclonal, Humanized; D000068258:Bevacizumab; D002057:Burns, Chemical / Q000150:complications*; D003228:Conjunctiva; D016510:Corneal Neovascularization / Q000209:etiology / Q000517:prevention & control*; D004195:Disease Models, Animal; D005126:Eye Burns / Q000139:chemically induced*; D007267:Injections; D011817:Rabbits; D012972:Sodium Hydroxide; D042461:Vascular Endothelial Growth Factor A / Q000037:antagonists & inhibitors
chemical_list: D020533:Angiogenesis Inhibitors; D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D042461:Vascular Endothelial Growth Factor A; D000068258:Bevacizumab; D012972:Sodium Hydroxide