Abstract
To evaluate the efficacy of prostaglandin antagonists on blood-retinal barrier breakdown induced by anterior segment intraocular simulated surgery. Rats were randomly assigned to a negative control group, model group, nonsteroidal anti-inflammatory drugs prophylactic treatment group, nonsteroidal anti-inflammatory drugs treatment group, corticosteroid prophylactic treatment group, and corticosteroid treatment group. Four hours and 48h after modeling, the concentrations of PGE1, PGE2, and PGF2 α in the aqueous humor and vitreous body of the rat model were visualized using ELISA. The integrity of the blood-retinal barrier was quantitatively measured using Evan's blue as a tracer. Four hours after modeling, the concentrations of PGE1, PGE2, and PGF2α in the aqueous humor and vitreous body in the negative control group and the nonsteroidal anti-inflammatory drugs prophylactic treatment group were significantly lower than those in the model group. The concentrations of PGE1, PGE2, and PGF2α in the aqueous humor and vitreous body in the corticosteroid prophylactic treatment group were higher than those in the negative control group and the nonsteroidal anti-inflammatory drugs prophylactic treatment group. Forty-eight hours after modeling, the concentrations of PGE1, PGE2, and PGF2α in the aqueous humor and vitreous body in the nonsteroidal anti-inflammatory drugs prophylactic treatment group, nonsteroidal anti-inflammatory drugs treatment group, corticosteroid prophylactic treatment group, and corticosteroid treatment group were lower than those in the model group, but higher than those in the negative group. Retinal Evan's blue leakage in the nonsteroidal anti-inflammatory drugs prophylactic treatment group was higher than that in the negative control group, and lower than those in the nonsteroidal anti-inflammatory drugs treatment group, corticosteroid prophylactic treatment group, corticosteroid treatment group, and model group. Retinal Evan's blue leakage in the nonsteroidal anti-inflammatory drugs treatment group, corticosteroid prophylactic treatment group, and corticosteroid treatment group were lower than those in the model group. This study confirms that prostaglandin antagonists can relieve blood-retinal barrier breakdown in a rat model and that nonsteroidal anti-inflammatory drugs prophylactic treatment can achieve better efficacy.
Highlights
Postoperative cystoid macular edema (CME) can occur following various types of intraocular surgery, such as cataract[1,2,3,4,5], trabeculectomy[6], and corneal transplanta tion[7,8]
Four hours after modeling, ELISA showed that the concentrations of PGE1, PGE2, and PGF2α in the aqueous humor and vitreous body in the negative control group were similar to those of the Nonsteroidal anti-inflammatory drugs (NSAIDs) pro phylactic treatment group
The diffe rences among the six groups were statistically significant (Aqueous humor PGE1: F=971.845, p
Summary
Postoperative cystoid macular edema (CME) can occur following various types of intraocular surgery, such as cataract[1,2,3,4,5], trabeculectomy[6], and corneal transplanta tion[7,8]. Cataract is the most common cause of blindness worldwide, leading to blindness for 10.8 million people and visual impairment for 35.1 million in 2010(9). Glau coma is the second most common cause of blindness worldwide, with 2.1 million cases of blindness, and 4.2 million cases of visual impairment resulting from glau coma in 2010(10). CME is the most common cause of poor visual outcome or visual distor tion following cataract surgery. The baseline incidence of pseudophakic CME was 1.17% in eyes without ope rative complications, diabetes, or risk factors. The risk was higher in the presence of any diabetic retinopathy, epiretinal membrane, uveitis, capsule rupture with or without vitreous loss, retinal vein occlusion, or retinal detachment repair[1]
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