ИСТИНА

Ocular inflammation may contribute to the pathogenesis of a number of blind-causing retinal disorders, including age-related macular degeneration and diabetic retinopathy, and may play a role in glaucoma. It can manifest in the aqueous humor (AH) as alterations in the content lipid mediators regulating inflammation and resolution pathways as well as neuronal survival. In this study, a model of glaucoma was induced in rabbits and the developing pathological process was characterized on clinical and electrophysiological levels as well as by lipidomic analysis of AH.Chronic intraocular hypertension was stimulated by single or double (with an interval of one week) injections of 2% methylcellulose in the anterior chamber. The intraocular pressure peaked at 4–5 hours after each injection and remained elevated for at least ten days yielding glaucoma-like neuronal damage as evidenced by electroretinography. The acute increase in intraocular pressure was accompanied by hyperemia of the precorneal vessels and corneal edema. The use of targeted lipidomic technique employing ultra-performance liquid chromatography-tandem mass spectrometry allowed identifying patterns of signaling lipids of AH, including polyunsaturated fatty acids, oxylipins, and phospholipid derivatives. The revealed glaucoma-related alterations in AH lipidome were indicative of oxidative stress and apparently low-grade ocular inflammation. Taken together, these findings provide a rationale for trialing a combination of antioxidant and anti-inflammatory therapies as a prospective route in the complex treatment of glaucoma. This study was supported by the Russian Science Foundation (Project no. 21-15-00123).