Abstract
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.
Highlights
REACTIVE OXYGEN SPECIES AS A TRIGGER OF THE INFARCT-LIMITING EFFECTS OF EARLY HYPOXIC PRECONDITIONING RAT MYOCARDIUM
The role of reactive oxygen species (ROS) in the signaling mechanism of the early hypoxic preconditioning 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
Summary
Исследование проводили на половозрелых крысах-самцах линии Wistar массой 300–350 г. Все болезненные процедуры осуществляли на наркотизированных животных, согласно рекомендациям о гуманном отношении к лабораторным животным, изложенным в «Правилах проведения работ с использованием экспериментальных животных», утвержденных Приказами МЗ СССР No 742 от 13.11.84 г. «Об утверждении правил проведения работ с использованием экспериментальных животных» и No 48 от 23.01.85 г. «О контроле за проведением работ с использованием экспериментальных животных». Подопытные группы включали крыс, которым за 15 мин перед рГП вводили низкомолекулярные водо- и жирорастворимые препараты-антиоксиданты: 1) 2-меркаптопропионилглицин (2-МПГ) в дозе 20 мг/кг (n = 15); 2) тролокс в дозе 2,5 мг/кг (n = 12); темпол в дозе. Одной группе подопытных 2-МПГ в дозе 20 мг/кг вводили через 30 мин после рГП (n = 14). После ишемии-реперфузии определяли размеры зоны некроза миокарда. Инфаркт-лимитирующий эффект оценивали по соотношению размеров зоны некроза к области риска, используя компьютеризированный планиметрический метод
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