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Purpose: This study aims to investigate the protective efficacy of nintedanib in experimental uveitis induced by endotoxins., Materials and Methods: In this study, 24 Wistar albino rats were randomly divided into three groups: Group I was the healthy control with no uveitis that did not receive any treatment, Group II (sham) group did not receive treatment, and Group III (nintedanib) received oral nintedanib for 10 days. On the 10th day, endotoxin-induced uveitis (EIU) was induced by lipopolysaccharide (LPS) injection in Groups II and III. The clinical activity score was evaluated in all groups at the 24th hour, when uveitis formation was thought to be the most intense after LPS injection. All rats were then killed via anaesthesia. Tumour necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) levels were measured in their right eyes using the enzyme-linked immunosorbent assay (ELISA) method. Further, histopathological examinations were performed on their left eyes., Results: For Groups I, II, and III, the IL-6 levels were 30.88 ± 1.79, 36.77 ± 1.21, and 30.93 ± 3.96 mg/pr, respectively, and TNF-α levels were 50.20 ± 3.24, 59.87 ± 2.98, and 50.23 ± 4.83 mg/pr, respectively. IL-6, TNF-α levels and clinical activity score were higher in the sham group compared to the other groups, and it decreased significantly in the treatment group ( p  < 0.05). Intense inflammatory cell infiltration of the ciliary body, edema and hyperaemia were evident in the sham group compared to the healthy control group ( p  < 0.05). These pathological findings were significantly decreased in the treatment group compared to the sham group ( p  < 0.05)., Conclusion: Nintedanib may be preferable as a new agent for treating non-infectious uveitis. However, further studies are needed to evaluate its long-term effects, effects on other antiinflammatory pathways, side-effects, and ideal dose optimization.

Purpose: To investigate the efficiency of intravitreal octreotide, which has previously been shown to have benefits in the treatment of proliferative vitreoretinopathy (PVR), and intravitreal infliximab as a novel option in an experimental dispase-induced PVR model. Methods: A total of 28 pigmented guinea pigs were divided into four groups, and each group consisted of seven subjects. Group 1 (control) was treated with a 0.2 mL saline solution intravitreally from 1.5 mm behind the limbus. Group 2 (sham) was treated with 0.07 IU/0.1 mL dispase 0.1 mL saline solution using the same method. Group 3(infliximab) received 0.07 IU/0.1 mL dispase and 1 mg/0.1 mL infliximab, and group 4(octreotide) was treated with 0.07 IU/0.1 mL dispase and 1 mg/0.1 mL octreotide. An intravitreal injection of infliximab and octreotide was administered to groups 3 and 4 two times during the experiment. The subjects were held for a 10-week period to await for the formation of PVR. At the end of ten weeks, the eyes were enucleated, and tumour necrosis factor-alpha (TNF-α), interleukin 1(IL-1), interleukin 6 (IL-6), transforming growth factor (TGF-β), and platelet-derived growth factor (PDGF) and levels in homogenised retina tissue were measured using the enzyme linked-immuno-sorbent assay (ELISA) method. Results: Retinal TNF-α, IL-1, IL-6, and PDGF levels had significantly decreased in treatment groups compared to the sham group ( p  < 0.05). The decrease in the level of TGF-β was not statistically significant between the treatment and the sham groups ( p  > 0.05). Conclusions: Intravitreal infliximab can inhibit the development of PVR and reduce levels of cytokine, which plays an essential role in the pathogenesis of PVR. The results of our study suggest that it may be possible to identify the ideal adjuvant pharmacological drugs that are effective in preventing PVR.