Use of caffeic acid phenethyl ester and cortisone may prevent proliferative vitreoretinopathy.

Yusuf Turkoz,Hakan Parlakpınar,Yılmaz Çigremis,Bülent Mızrak,Hamdi Er,Harun Yılmaz,Mehmet Borazan

doi:10.1080/09629350410001688512

Yusuf Turkoz, Hakan Parlakpınar + Show 5 more

Open Access

https://doi.org/10.1080/09629350410001688512

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Abstract

PURPOSE: To investigate whether caffeic acid phenethyl ester (CAPE) and cortisone prevent proliferative vitreoretinopathy (PVR). METHODS: Twenty pigmented rabbits were used in this study. All rabbits except controls received an intravitreal injection of 0.15 ml (75,000 U) of platelet-rich plasma into their left eye. The animals were divided into four groups: group I was treated with intraperitoneal injection of 0.5 ml (15 micromol/kg) of CAPE for 3 days, group II received 0.15 ml (4 mg/kg) of intravitreal cortisone, group III received nothing (blank group), and group IV (control group) received only 1 ml of 1% ethanol intraperitoneally daily for 3 days. Proliferative changes were graded in a masked fashion by indirect ophthalmoscopy for a 15-day follow-up period. The malondialdehyde (MDA), reduced glutathione (GSH) and total nitrite (NO) levels were measured in the vitreous humor. RESULTS: The grades of PVR were B-C in group I, and C-D in group II. The PVR grade in the control group was C-D. The mean MDA level in group I (4.0+/-0.8 micromol/l) was significantly lower than in the blank group (6.0 micromol/l) (p < 0.05). The mean GSH level in group I (71.0+/-11.2 micromol/l) was significantly different than in the blank group (p < 0.05). The MDA and GSH levels in group II were 4.7+/-0.6 micromol/l and 53.8+/-7.8 micromol/l, respectively. Both these levels were not significantly different from the blank group (p > 0.05). The NO levels in both treatment groups were significantly lower than in the blank group (p < 0.001). CONCLUSION: These findings suggest an inhibitory effect of CAPE on PVR. The inhibitory effect was supported by lower MDA and NO with higher GSH levels in treatment groups than in the blank group. There was no detected significant effect of cortisone for preventing PVR experimentally.

Highlights

Proliferative vitreoretinopathy (PVR) is a complex process involving inflammation, migration and proliferation of retinal pigment epithelial cells.[1,2] Several inflammatory cytokines and growth factors are involved in these processes
The animals were divided into four groups: group I was treated with intraperitoneal injection of 0.5 ml (15 mmol/kg) of caffeic acid phenethyl ester (CAPE) for 3 days, group II received 0.15 ml (4 mg/ml) of intravitreal cortisone, group III received nothing, and group IV received only 1 ml of 1% ethanol intraperitoneally daily for 3 days
NO levels in the vitreous humor of groups I and II were significantly lower than the blank group

Summary

Introduction

Proliferative vitreoretinopathy (PVR) is a complex process involving inflammation, migration and proliferation of retinal pigment epithelial cells.[1,2] Several inflammatory cytokines and growth factors are involved in these processes. PVR is the most common cause of failure in the treatment of retinal detachment and other vitreoretinal procedures. Previous studies have shown that different pharmacologic therapies may modify the proliferative process and improve the success of surgery.[3,4] The migration of retina pigment epithelial cells is an important step in PVR. Blockage of the retina pigment epithelial cell migration might be useful in preventing proliferation

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