actabiomedicaActa Biomedica ScientificaActa Biomedica Scientifica2541-94202587-9596Scientific Centre for Family Health and Human Reproduction Problems10.12737/article_590823a507e6d8.99508073actabiomedica-204Research ArticleЭКСПЕРИМЕНТАЛЬНЫЕ ИССЛЕДОВАНИЯ В БИОЛОГИИ И МЕДИЦИНЕEXPERIMENTAL RESEARCHES IN BIOLOGY AND MEDICINEАктивные формы кислорода как триггеры инфаркт-лимитирующего эффекта раннего гипоксического прекондицио-нирования миокарда крысыReactive oxygen species as a trigger of the infarct-limiting effects of early hypoxic preconditioning rat myocardiumСеменцовА. С.SementsovA. S.hamkot@sibmail.comКрылатовА. В.KrylatovA. V.noemail@neicon.ruФГБНУ «Научно-исследовательский институт кардиологии»Research Institute for Cardiology20162805201613(2)128130Copyright © Семенцов А.С., Крылатов А.В., 20162016Семенцов А.С., Крылатов А.В.Sementsov A.S., Krylatov A.V.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://www.actabiomedica.ru/jour/article/view/204

Исследовали роль активных форм кислорода в сигнальном механизме раннего гипоксического прекондиционирования (рГП) in vivo. Установили, что предварительное введение неселективного антиоксиданта непрямого действия N-(2-меркаптопропионил)-глицина и «ловушки» гидроксильных радикалов 1,3-диметилтиомочевины полностью устраняло инфаркт-лимитирующий эффект адаптации. Введение антиоксидантов темпол и тролокс, а также применение N-(2-меркаптопропионил)-глицина после рГП не оказывало влияния на защитный эффект адаптации.

It is believed that reactive oxygen species (ROS) are involved in the performance of this adaptive hepatoprotective effect phenomenon. However, the role of ROS in the signaling mechanism of the early hypoxic preconditioning (early HP) and the contribution of individual types of oxygen radicals in the infarct-limiting effect of early HP remains uncertain to the end. Objective was to investigate the role of various types of reactive oxygen species in the signaling mechanism of the infarct-limiting effect of early hypoxic preconditioning. We investigated the role of reactive oxygen species in the signaling mechanism of early HP in vivo. Adaptation of animals was conducted with 6 transient hypoxia-reoxygenation sessions before prolonged ischemia (45 min) and reperfusion (120 min). Low molecular weight antioxidants were administered 15 minutes prior to the HP. We found out that pretreatment with the nonselective antioxidant indirect action of N-(2-mercaptopropionyl)-glycine and "trap" of hydroxyl radicals 1,3-dimethylthiourea completely eliminated the infarct-limiting effect of adaptation. Administration of antioxidants tempol and trolox, as well as the use of N-(2-mercaptopropionyl)-glycine after HP had no effect on the protective effect of adaptation. Consequently, reactive oxygen species, including hydroxyl radical, operate as the trigger function in the signaling mechanism of early HP.

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