vestnik-bio-msuВестник Московского университета. Серия 16. БиологияVestnik Moskovskogo universiteta. Seriya 16. Biologiya0137-0952Lomonosov Moscow State University, School of Biologyvestnik-bio-msu-657Research ArticleОБЗОРREVIEWРОЛЬ АКТИВНЫХ ФОРМ КИСЛОРОДА В ВОСПАЛЕНИИ. МИНИ-ОБЗОРTHE ROLE OF REACTIVE OXYGEN SPECIES IN INFLAMMATION. MINI-REVIEWЧеломбитькоМ. А.ChelombitkoM. A .

119234, г. Москва, Ленинские горы, д. 1, стр. 12

мл. науч. сотр. кафедры клеточной биологии и гистологии биологического факультета.

Тел.: 8-495-939-45-67

Department of Cell Biology and Histology, School of Biology

Leninskiye gory 1–12, Moscow, 119234

chelombitko@mail.bio.msu.ruМосковский государственный университет имени М.В. ЛомоносоваРоссияLomonosov Moscow State UniversityRussian Federation201829112018734242246Copyright © Челомбитько М.А., 20182018Челомбитько М.А.Chelombitko M.A.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://vestnik-bio-msu.elpub.ru/jour/article/view/657

Воспаление представляет собой защитную реакцию многоклеточного организма на повреждение, направленную на локализацию, уничтожение и удаление повреждающего агента, а также на восстановление (или замещение) поврежденных им тканей. В последнее время появляется все больше данных, свидетельствующих об участии активных форм кислорода (АФК) в инициации, развитии и завершении воспалительной реакции. При этом АФК выступают в качестве бактерицидных агентов и “вторичных мессенджеров” при внутриклеточной передаче сигналов. Последнюю функцию они выполняют посредством посттрансляционной модификации белков, содержащих в своем составе редокс-чувствительные остатки цистеина, которые могут подвергаться окислению. В то же время известно, что чрезмерная продукция АФК может привести к серьезному повреждению клеток и тканей и способствовать хронизации воспаления, лежащего в основе многих нейродегенеративных, сердечно-сосудистых и метаболических заболеваний. В настоящей работе рассматриваются сведения об участии АФК в ключевых этапах воспалительного процесса (увеличении проницаемости стенки сосудов и миграции лейкоцитов, респираторном взрыве и фагоцитозе, ангиогенезе), а также некоторых из событий, ведущих к завершению воспаления. Помимо этого, рассматривается патологическая роль АФК при окислительном стрессе.

Inflammation is a protective response of a multicellular organism to injury. The function of inflammation is to localize and eliminate harmful stimuli, as well as repair (or replace) damaged tissues. There is increasing evidence that reactive oxygen species (ROS) participate in the initiation, progression and resolution of an inflammatory reaction. In this case, ROS act as bactericidal agents and “second messengers” in intracellular signaling. The latter function is performed by post-translational modification of proteins containing redox-sensitive cysteine residues, which are susceptible to oxidation. At the same time, overproduction of ROS can lead to cell and tissue injury and contribute to chronic inflammation underlying many neurodegenerative, cardiovascular and metabolic diseases. In this review, we focus on the role of ROS in critical inflammatory events, including increased vascular permeability and leukocyte extravasation, respiratory burst and phagocytosis, angiogenesis, as well as some events leading to the resolution of inflammation. In addition, we discuss the pathological role of ROS in oxidative stress.

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The authors declare that there are no conflicts of interest present.