Effect of the Toll-Like Receptor 4 Antagonist Eritoran on Retinochoroidal Inflammatory Damage in a Rat Model of Endotoxin-Induced Inflammation
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). Gr...
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| Format: | Article |
| Language: | English |
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Wiley
2014-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2014/643525 |
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| author | Feyzahan Ekici Emine Esra Karaca Şafak Korkmaz Osman Yüksel Özlem Gülbahar Murat Alper Sevim Ercan Meral Or |
| author_facet | Feyzahan Ekici Emine Esra Karaca Şafak Korkmaz Osman Yüksel Özlem Gülbahar Murat Alper Sevim Ercan Meral Or |
| author_sort | Feyzahan Ekici |
| collection | DOAJ |
| description | 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. |
| format | Article |
| id | doaj-art-005ce86f1507448b94a59fd498624d10 |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2014-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-005ce86f1507448b94a59fd498624d102025-02-03T05:47:16ZengWileyMediators of Inflammation0962-93511466-18612014-01-01201410.1155/2014/643525643525Effect of the Toll-Like Receptor 4 Antagonist Eritoran on Retinochoroidal Inflammatory Damage in a Rat Model of Endotoxin-Induced InflammationFeyzahan Ekici0Emine Esra Karaca1Şafak Korkmaz2Osman Yüksel3Özlem Gülbahar4Murat Alper5Sevim Ercan6Meral Or7Department of Ophthalmology, Recep Tayyip Erdogan University Medical School, 53020 Rize, TurkeyDepartment of Ophthalmology, Sorgun State Hospital, 66700 Yozgat, TurkeyDepartment of Ophthalmology, Duzce State Hospital, 81100 Duzce, TurkeyDepartment of General Surgery, Gazi University Medical School, 06560 Ankara, TurkeyDepartment of Medical Biochemistry, Gazi University Medical School, 06560 Ankara, TurkeyDepartment of Pathology, Dışkapı Training and Research Hospital, 06330 Ankara, TurkeyDepartment of Medical Pharmacology, Gazi University Medical School, 06560 Ankara, TurkeyDepartment of Ophthalmology, Gazi University Medical School, 06560 Ankara, TurkeyPurpose. 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.http://dx.doi.org/10.1155/2014/643525 |
| spellingShingle | Feyzahan Ekici Emine Esra Karaca Şafak Korkmaz Osman Yüksel Özlem Gülbahar Murat Alper Sevim Ercan Meral Or Effect of the Toll-Like Receptor 4 Antagonist Eritoran on Retinochoroidal Inflammatory Damage in a Rat Model of Endotoxin-Induced Inflammation Mediators of Inflammation |
| title | Effect of the Toll-Like Receptor 4 Antagonist Eritoran on Retinochoroidal Inflammatory Damage in a Rat Model of Endotoxin-Induced Inflammation |
| title_full | Effect of the Toll-Like Receptor 4 Antagonist Eritoran on Retinochoroidal Inflammatory Damage in a Rat Model of Endotoxin-Induced Inflammation |
| title_fullStr | Effect of the Toll-Like Receptor 4 Antagonist Eritoran on Retinochoroidal Inflammatory Damage in a Rat Model of Endotoxin-Induced Inflammation |
| title_full_unstemmed | Effect of the Toll-Like Receptor 4 Antagonist Eritoran on Retinochoroidal Inflammatory Damage in a Rat Model of Endotoxin-Induced Inflammation |
| title_short | Effect of the Toll-Like Receptor 4 Antagonist Eritoran on Retinochoroidal Inflammatory Damage in a Rat Model of Endotoxin-Induced Inflammation |
| title_sort | effect of the toll like receptor 4 antagonist eritoran on retinochoroidal inflammatory damage in a rat model of endotoxin induced inflammation |
| url | http://dx.doi.org/10.1155/2014/643525 |
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