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Nagehan Can,1 Onur Catak,2 Burak Turgut,2 Tamer Demir,2 Nevin Ilhan,3 Tuncay Kuloglu,4 Ibrahim Hanifi Ozercan5 1Department of Ophthalmology, Elaziğ Training and Research Hospital, 2Department of Ophthalmology, 3Department of Biochemistry, 4Department of Histology and Embryology, 5Department of Pathology, School of Medicine, Firat University, Elaziğ, Turkey Abstract: Damage to retinal ganglion cells due to elevation of intraocular pressure (IOP) is responsible for vision loss in glaucoma. Given that loss of these cells is irreversible, neuroprotection is crucial in the treatment of glaucoma. In this study, we investigated the possible antioxidant and neuroprotective effects of ghrelin on the retina in an experimental glaucoma model. Twenty-one Sprague–Dawley rats were randomly assigned to three groups comprising seven rats each. The rats in the control group were not operated on and did not receive any treatment. In all rats in the other groups, IOP was increased by cauterization of the limbal veins. After creation of the IOP increase, saline 1 mL/kg or ghrelin 40 µg/kg was administered intraperitoneally every day for 14 days in the vehicle control group and ghrelin groups, respectively. On day 14 of the study, the eyes were enucleated. Levels of malondialdehyde (MDA), nitric oxide (NO), and nitric oxide synthase-2 (NOS2) in anterior chamber fluid were measured. The retinas were subjected to immunohistochemistry staining for glial fibrillary acidic protein (GFAP), S-100, and vimentin expression. Mean levels of MDA, NO, and NOS2 in the aqueous humor were higher in the vehicle control group than in the control group (P0.05). Retinal TUNEL and immunohistochemistry staining in the vehicle control group showed an increase in apoptosis and expression of GFAP, S-100, and vimentin compared with the control group (P

Burak Turgut,1 Kenan Eren,1 Mehmet Mustafa Akin,2 Tamer Demir,1 Sabiha Kobat1 1Department of Ophthalmology, School of Medicine, Firat University, Elaziğ, Turkey; 2Department of Pathology, School of Medicine, Firat University, Elaziğ, Turkey Background: The purpose of this work was to look into the effects of infliximab on wound healing in experimental glaucoma filtration surgery and to compare the antifibrotic effects of this agent to that of mitomycin-C (MMC). Methods: Twenty-eight male New Zealand White rabbits were randomly assigned to four groups, each including seven rabbits: control group, sham group, MMC group, and infliximab group. The rabbits in the control group were not operated on and did not receive any treatment. The rabbits in the sham group underwent trabeculectomy and had one drop of saline instilled four times a day for 14 days. The rabbits in the MMC treatment group underwent trabeculectomy, and a sponge soaked in 0.4 mg/mL MMC was applied intraoperatively to the scleral surgical site for three minutes. The rabbits in the infliximab treatment group underwent trabeculectomy and one drop of 10 mg/mL infliximab was instilled four times a day for 14 days after surgery. On day 14 of the experiment, the operated and control eyes were enucleated and histologically and immunohistochemically analyzed. Results: The mean fibroblast and mononuclear cell (MNC) numbers and the mean immunostaining intensities of transforming growth factor-β (TGF-β), fibroblast growth factor-β (FGF-β), and platelet-derived growth factor (PDGF) in the sham group were higher than those of the control group (P0.05). Conclusion: Our study suggests that topical infliximab effectively suppresses the subconjunctival wound healing response after experimental glaucoma filtration surgery, reducing the MNC and fibroblast numbers and immunostaining intensities of TGF-β, FGF-β, and PDGF. Keywords: mitomycin-C, trabeculectomy, anti-TNF, growth factors

Burak Turgut,1 Fatih Cem Gül,1 Ferda Dağli,2 Nevin Ilhan,3 Metin Özgen41Department of Ophthalmology, School of Medicine, Firat University, Elazig, 2Department of Pathology, School of Medicine, İnönü University, Malatya, 3Department of Biochemistry, School of Medicine, Firat University, Elazig, 4Department of Rheumatology, School of Medicine, İnönü University, Malatya, TurkeyBackground: 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.Methods: 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.Results: 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).Conclusion: Ghrelin failed to decrease the IL-1, IL-6, and TNF-α levels that play a critical role in the pathogenesis of uveitis.Keywords: uveitis, tumor necrosis factor-alpha, interleukin-1, interleukin-6, infliximab, ghrelin

OBJECTIVE: There is more pronounced hypercoagulation in COVID-19 infection than in other viral lung infections. Oxidized phospholipids (OxPLs) appear in COVID-19-infected lungs due to oxidative stress, after which they promote the induction of tissue factor (TF) expression and inflammatory programmers in monocytes, as well as activate endothelial cells to recruit and bind to monocytes. Therefore, we aimed to demonstrate the role of OxPLs in inflammatory and procoagulant responses in COVID-19 infection. PATIENTS AND METHODS: Patients with a positive SARS-CoV-2 polymerase chain reaction test and ten healthy donors were included in the study. Peripheral blood was drawn at inclusion for OxPAPC, IFN-γ, and CCL2 serum level measurements. Clinical data were collected from electronic patient medical files. The serum levels of OxPAPC, IFNγ, and CCL2 were measured by immune assays. RESULTS: Seventy-two patients were included in the study. OxPAPC and CCL2 were higher in the patients than in the controls (<0.003 and 0.011, respectively). INF-γ did not significantly differ between groups. There was no difference between the patients with lung involvement and those without CCL2, INF-γ, and OxPAPC. D-dimer, CRP, and ferritin were higher in the patients with lung involvement. Serum levels of INF-γ and CCL2 were positively correlated with each other (r:0.757, p<0.0001), but no correlation was detected between OxPAPC and INF-γ or CCL2. There was no correlation between OxPAPC and hematologic or biochemical parameters. CONCLUSIONS: OxPAPC, which is thought to contribute to hypercoagulability, was found to be high in the patients with Covid-19 infection. The role of OxPLs in COVID-19-associated hypercoagulopathy should be investigated further in experimental models and in larger patient groups. [ABSTRACT FROM AUTHOR]