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Mediators of Inflammation
Volume 2014 (2014), Article ID 643525, 9 pages
http://dx.doi.org/10.1155/2014/643525
Research Article

Effect of the Toll-Like Receptor 4 Antagonist Eritoran on Retinochoroidal Inflammatory Damage in a Rat Model of Endotoxin-Induced Inflammation

1Department of Ophthalmology, Recep Tayyip Erdogan University Medical School, 53020 Rize, Turkey
2Department of Ophthalmology, Sorgun State Hospital, 66700 Yozgat, Turkey
3Department of Ophthalmology, Duzce State Hospital, 81100 Duzce, Turkey
4Department of General Surgery, Gazi University Medical School, 06560 Ankara, Turkey
5Department of Medical Biochemistry, Gazi University Medical School, 06560 Ankara, Turkey
6Department of Pathology, Dışkapı Training and Research Hospital, 06330 Ankara, Turkey
7Department of Medical Pharmacology, Gazi University Medical School, 06560 Ankara, Turkey
8Department of Ophthalmology, Gazi University Medical School, 06560 Ankara, Turkey

Received 23 March 2014; Revised 29 May 2014; Accepted 29 May 2014; Published 17 June 2014

Academic Editor: Andrzej Grzybowski

Copyright © 2014 Feyzahan Ekici et al. 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. We investigated the effect of eritoran, a Toll-like receptor 4 antagonist, on retinochoroidal inflammatory damage in an endotoxin-induced inflammatory rat model. Methods. Endotoxin-induced inflammatory model was obtained by intraperitoneal injection of 1.5 mg/kg lipopolysaccharide (LPS). Group 1 had control rats; in groups 2-3 LPS and 0.5 mg/kg sterile saline were injected; and in groups 4-5 LPS and 0.5 mg/kg eritoran were injected. Blood samples were taken and eyes were enucleated after 12 hours (h) (groups 2 and 4) or 24 hours (Groups 3 and 5). Tumor necrosis factor-α (TNF-α) and malondialdehyde (MDA) levels in the serum and retinochoroidal tissue and nuclear factor kappa-B (NFκB) levels in retinochoroidal tissue were determined. Histopathological examination was performed and retinochoroidal changes were scored. Results. Eritoran treatment resulted in lower levels of TNF-α, MDA, and NFκB after 12 h which became significant after 24 h. Serum TNF-α and retinochoroidal tissue NFκB levels were similar to control animals at the 24th h of the study. Eritoran significantly reversed histopathological damage after 24 h. Conclusions. Eritoran treatment resulted in less inflammatory damage in terms of serum and retinochoroidal tissue parameters.