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      Impact of ghrelin on vitreous cytokine levels in an experimental uveitis model

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          The purpose of this study was to investigate the effect of intraperitoneal ghrelin on vitreous levels of interleukin (IL)-1, IL-6, and tumor necrosis factor-alpha (TNF-α) and to compare its effects with those of intraperitoneal infliximab in an experimental uveitis model.


          Twenty-four male rats were assigned to four groups of six rats in each. All the rats, except for those in group 1 (controls), were injected intravitreally with concanavalin A to induce experimental uveitis. Rats in group 2 (sham) were not given any treatment after uveitis was induced. Rats in group 3 were given intraperitoneal infliximab 0.5 mg/100 mL on days 0, 1, 3, 5, and 7 following induction of uveitis on day 14 of the study. Rats in group 4 were given intraperitoneal ghrelin 10 ng/kg/day for 7 days following induction of uveitis. On day 21 of the study, enucleated globes were subjected to histopathologic examination. Vitreous levels of IL-1, IL-6, and TNF-α were measured by enzyme-linked immunosorbent assay.


          Vitreous levels of IL-1, IL-6, and TNF-α were significantly increased in the sham group relative to the control group ( P < 0.05), but showed a significant decrease in the group treated with infliximab ( P < 0.05). Cytokine levels also decreased in the ghrelin-treated group, but the decrease was not statistically significant ( P > 0.05).


          Ghrelin failed to decrease the IL-1, IL-6, and TNF-α levels that play a critical role in the pathogenesis of uveitis.

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          Most cited references 20

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          Cytokines and uveitis, a review.

          Although the exact pathogenic mechanisms underlying uveitis are unknown, cytokines appear to be involved in this inflammatory disorder. This review describes the studies in which the uveitogenic properties of several cytokines, including tumor necrosis factor (TNF), interleukin 1 (IL-1), IL-6, IL-8 and interferon gamma (IFN-gamma), were investigated and the reports on intraocular expression of cytokines, such as TNF, IL-2, IL-6 and IFN-gamma, during uveitis. The exact contribution of these mediators to uveitis remains to be determined. This may provide new clues in the treatment of uveitis.
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            The immuno-inflammatory cascade.

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              Plasma and aqueous humour levels of ghrelin in open-angle glaucoma patients.

              To compare aqueous humour and plasma levels of ghrelin, a peptide recently identified in human eyes, in patients with open-angle glaucoma and controls. Cross-sectional, controlled, hospital-based study. Twenty-four open-angle glaucoma (17 primary open-angle and 7 pseudo-exfoliation glaucoma) patients and 30 controls were included. All participants were patients scheduled for cataract or glaucoma surgery. Patients with other ocular pathology, previous ocular surgery or diabetes were excluded. Blood samples were collected before elective surgery. Aqueous humour was aspirated from the anterior chamber through a paracentesis with a 27-G needle under sterile conditions before any tissue manipulation. Ghrelin quantification was performed with commercially available Radioimmunoassay kits. Ghrelin levels in aqueous humour and plasma. Plasma levels of ghrelin were 490.5 ± 156.0 pg/mL in the open-angle glaucoma and 482.2 ± 125.4 pg/mL in the control group (Mann-Whitney test, P = 0.897). Aqueous humour levels of ghrelin were 85.5 ± 15.4 and 123.4 ± 25.5 pg/mL in the respective groups (P < 0.001). The ratio of plasma/aqueous humour ghrelin concentration was higher in the open-angle glaucoma versus the control group (5.75 ± 1.92 vs. 4.00 ± 1.04, P < 0.001). There was no difference in aqueous humour levels of ghrelin between primary open-angle glaucoma and pseudo-exfoliation glaucoma patients (P = 0.494). Aqueous humour levels of ghrelin were significantly lower in open-angle glaucoma patients, compared with controls. This difference may manifest a role of ghrelin in the disease process or a consequence of antiglaucoma treatment. © 2011 The Authors. Clinical and Experimental Ophthalmology © 2011 Royal Australian and New Zealand College of Ophthalmologists.

                Author and article information

                Drug Des Devel Ther
                Drug Des Devel Ther
                Drug Design, Development and Therapy
                Dove Medical Press
                09 January 2013
                : 7
                : 19-24
                [1 ]Department of Ophthalmology, School of Medicine, Fırat University, Elazig
                [2 ]Department of Pathology, School of Medicine, İnönü University, Malatya
                [3 ]Department of Biochemistry, School of Medicine, Fırat University, Elazig
                [4 ]Department of Rheumatology, School of Medicine, İnönü University, Malatya, Turkey
                Author notes
                Correspondence: Burak Turgut, Fırat University School of Medicine, Department of Ophthalmology, Elazığ, Turkey, Tel +90 42 4233 3555, Fax +90 42 4238 8096, Email drburakturgut@ 123456gmail.com
                © 2013 Turgut et al, publisher and licensee Dove Medical Press Ltd.

                This is an Open Access article which permits unrestricted noncommercial use, provided the original work is properly cited.

                Original Research


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