Simavlı, HüseyinErdurmuş, MesutTerzi, Elçin HakanBucak, Yasin YücelÖnder, Halil İbrahimKükner, Ahmet Şahap2020-04-302020-04-3020141080-76831557-7732https://doi.org/10.1089/jop.2013.0238https://hdl.handle.net/20.500.12684/4832Simavli, Huseyin/0000-0003-1657-9099WOS: 000342560200007PubMed: 24983781Purpose: To evaluate the inhibitory effects of propranolol, a nonselective and lipophilic -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 1mg/mL, Group III received propranolol hydrochloride 1mg/mL, and Group IV received 0.5mg/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 0.5mg/mL does not have a significant inhibitory effect on alkali-induced corneal NV in rats.en10.1089/jop.2013.0238info:eu-repo/semantics/closedAccessArticle308650656WOS:000342560200007Q2Q3