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Mediators of Inflammation
Volume 13 (2004), Issue 2, Pages 127-130
http://dx.doi.org/10.1080/09629350410001688512

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

1Department of Biochemistry, Inonu University Turgut Ozal Medical Center, Malatya 44069, Turkey
2Department of Ophthalmology, Inonu University Turgut Ozal Medical Center, Malatya 44069, Turkey
3Department of Pathology, Inonu University Turgut Ozal Medical Center, Malatya 44069, Turkey
4Department of Pharmacology, Inonu University Turgut Ozal Medical Center, Malatya 44069, Turkey
5Department of Biology, Inonu University Turgut Ozal Medical Center, Malatya 44069, Turkey

Copyright © 2004 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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 μmol/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 μmol/l) was significantly lower than in the blank group (6.0 μmol/l) (p<0.05). The mean GSH level in group I (71.0±11.2 μmol/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 μmol/l and 53.8±7.8 μmol/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.