title: The effect of β receptor blockade through propranolol on corneal neovascularization.
abstract: OBJECTIVE
  To evaluate the inhibitory effects of propranolol, a nonselective and lipophilic β-adrenergic receptor blocker, on alkali-induced corneal neovascularization (NV).
  
  
  METHODS
  Corneal NV was induced in 24 eyes of 24 Wistar rats using NaOH. Following alkali burn, animals were randomized into 4 groups according to topical treatment. Group I received 0.9% NaCl, Group II received preservative-free dexamethasone sodium phosphate 1 mg/mL, Group III received propranolol hydrochloride 1 mg/mL, and Group IV received 0.5 mg/mL propranolol hydrochloride drops twice a day for 7 days. The inhibitory effects of the drugs were compared as the percent areas of cornea covered by NV. Anti-vascular endothelial growth factor (VEGF) and anti-active caspase-3 immunostainings were also performed in corneal sections.
  
  
  RESULTS
  The median percent area of corneal NV was 59% (40.3-65.6) in Group I, 25.5% (20.9-43.4) in Group II, 68.9% (36.7-78.0) in Group III, and 50.4% (42.2-63.3) in Group IV. Group III and IV did not show any difference in comparison to Group I. Group II showed a statistically significant smaller area of corneal NV compared with Group I, III, and IV (P=0.004 for each comparison). Anti-VEGF immunostaining was significantly less in Group II compared with the other groups. Anti-active caspase-3 immunostaining was not different among the treatment groups.
  
  
  CONCLUSIONS
  Topical propranolol 1 or 0.5 mg/mL does not have a significant inhibitory effect on alkali-induced corneal NV in rats.
authors.affiliation: 1 Ophthalmology Clinic, Izzet Baysal State Hospital , Bolu, Turkey .
authors.forename: Hüseyin
authors.initials: H
authors.lastname: Simavli
authors.forename: Mesut
authors.initials: M
authors.lastname: Erdurmus
authors.forename: Elçin Hakan
authors.initials: EH
authors.lastname: Terzi
authors.forename: Yasin Yücel
authors.initials: YY
authors.lastname: Bucak
authors.forename: Halil İbrahim
authors.initials: Hİ
authors.lastname: Önder
authors.forename: Ahmet Şahap
authors.initials: AŞ
authors.lastname: Kükner
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*; D000818:Animals; D002057:Burns, Chemical / Q000150:complications; D053148:Caspase 3 / Q000378:metabolism; D002424:Caustics / Q000494:pharmacology; D016510:Corneal Neovascularization / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism; D003907:Dexamethasone / Q000008:administration & dosage / Q000627:therapeutic use; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D005126:Eye Burns / Q000139:chemically induced / Q000150:complications; D005938:Glucocorticoids / Q000008:administration & dosage / Q000627:therapeutic use; D007322:Instillation, Drug; D008297:Male; D011433:Propranolol / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*; D017208:Rats, Wistar; D012972:Sodium Hydroxide / Q000494:pharmacology; D016896:Treatment Outcome; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism
chemical_list: D000319:Adrenergic beta-Antagonists; D002424:Caustics; D005938:Glucocorticoids; D042461:Vascular Endothelial Growth Factor A; C467498:vascular endothelial growth factor A, rat; D012972:Sodium Hydroxide; D003907:Dexamethasone; D011433:Propranolol; C505410:Casp3 protein, rat; D053148:Caspase 3