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Influence of anti-inflammatory therapy on the nuclear/cell migration in retina in models of proliferative vitreoretinopathy and total retinal ischemia in rats

Keywords:

A.K. Erdiakov – Ph.D. (Biol.), Senior Research Scientist, Interfaculty Research Laboratory of Adaptation Medicine, Faculty of Fundamental Medicine, Lomonosov Moscow State University
E-mail: alexey.erdyakov@ya.ru
M.V. Tikhonovich – Ph.D. (Med.), Ophthalmologist, Hospital of the Presidential Property Management Department of the Russian Federation
E-mail: marina.tikhonovich@gmail.com
E.M. Klochikhina – Post-graduate Student, Department of Physiology and General Pathology, Faculty of Fundamental Medicine, Lomonosov Moscow State University
E-mail: klochikhinaem@gmail.com
O. Budarina – Student, Faculty of Fundamental Medicine, Lomonosov Moscow State University
E-mail: elena_budarin@yahoo.co.uk
S.A. Gavrilova – Ph.D. (Biol.), Associate Professor, Department of Physiology and General Pathology, Faculty of Fundamental Medicine, Lomonosov Moscow State University
E-mail: sgavrilova@mail.ru


Proliferative vitreoretinopathy (PVR) is a disease of the retina that can be seen as a healing reaction to the retinal damage. PVR is linked to activation of inflammation and development of fibrous membranes. It has previously been shown that intravitreal injection of the enzyme dispase (D) or lectin concanavalin A (ConA) leads to the development of the intraocular inflammation and PVR in rats and is accompanied by remodelling of the retina. One of the key morphological and histo-logical characteristics of retinal remodeling is the presence of nuclei in its non-nuclear layers. This phenomenon is called migration, and it illustrates the movement of retinal cells, or their nuclei. The present study aimed to systematically investigate migration of nuclei/cells at different stages of development of PVR, the impact of ischemia on the process of migration and the influence of anti-inflammatory therapy on the phenomenon of migration.
In total, 230 normal adult male albino rats (350 ± 50 g) were enrolled in this experiment. A PVR rat models were established by an intravitreal injection either of 2μl of dispase (0.015 U/μl) or of 2μl of concanavalin A solution (ConA) (0.25mg/ml) into the right eye under sterile conditions. 20 minutes later, an intraocular injection either of 2 μl of lornoxicam (8 mg/ml) or 2 μl of triamcinolone (40 mg/ml) was administered. On the 2nd and 3rd days after the initial injection of dispase or of concanavalin A, appropriate drugs were administered systemically. Lornoxicam was delivered intraperitoneally at a dose of 230 mg/kg, while triamcinolone was administered intramuscularly at a dose of 571 mg/kg. A rat model of irreversible retinal ischemia was induced by occlusion of a. carotis interna. Two ligatures were applied to a. carotis interna on anaesthesised animals (directly above the bifurcation of the carotid artery).
The obtained results confirmed the significance of the prostaglandins, components of arachidonic acid metabolism, in the regulation of the retinal cell activity demonstrating perspectives of using inhibitors of cyclooxygenases as a method of prevention and treatment of PVR. The ischemic component of the inflammatory reaction is not the main factor in the activation of migration processes in the retina. Retinoprotective properties of lornoxicam can be a potential prophylaxis for proliferative vitreoretinopathy, as well as a therapeutic agent in ischemic retinal diseases.

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May 29, 2020

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