Journal of ocular pharmacology and therapeutics : the official journal of the Association for Ocular Pharmacology and Therapeutics · 2014
The effect of β receptor blockade through propranolol on corneal neovascularization.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
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Simavli Hüseyin, Erdurmus Mesut, Terzi Elçin Hakan, Bucak Yasin Yücel, Önder Halil İbrahim, Kükner Ahmet Şahap
Аннотация
PURPOSE: 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.
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.