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Alterations in lipid mediators of inflammation associated with glaucomatous damage in a rabbit modelтезисы доклада
- Авторы: Tiulina V., Chistyakov D., Komarov S., Goriainov S., Gancharova O., Baksheeva V., Philippov P., Jr A.Zamyatnin, Iomdina E., Sergeeva M., Senin I., Zernii E.
- Сборник: FEBS Open Bio
- Серия: Suppl. S1
- Том: 11
- Тезисы
- Год издания: 2021
- Место издания: Wiley
- Первая страница: 505
- Последняя страница: 505
- Аннотация: Ocular inflammation may contribute to the pathogenesis of a number of blindcausing retinal disorders, including agerelated 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 45 hours after each injection and remained elevated for at least ten days yielding glaucomalike 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 ultraperformance liquid chromatographytandem mass spectrometry allowed identifying patterns of signaling lipids of AH, including polyunsaturated fatty acids, oxylipins, and phospholipid derivatives. The revealed glaucomarelated alterations in AH lipidome were indicative of oxidative stress and apparently lowgrade ocular inflammation. Taken together, these findings provide a rationale for trialing a combination of antioxidant and antiinflammatory therapies as a prospective route in the complex treatment of glaucoma. This study was supported by the Russian Science Foundation (Project no. 211500123).
- Добавил в систему: Ганчарова Ольга Сергеевна