Мітопротективний ефект Ронколейкіну при корекції експериментальних постгіпоксичних станів у щурів

Abstract

На модели экспериментального фотоиндуцированного тромбоза сосудов головного мозга у крыс изучена митопротекторная активность Ронколейкина(0,01 мг/кг) в сравнении с Тиотриазолином (50 мг/кг). На фоне применения Ронколейкина отмечена достоверная стабилизация функциональной активности митохондрий (по блокированию открытия митохондриальных пор) и состояния тиол-дисульфидной системы - нормализация активности глутатионпероксидазы и глутатионредуктазы, повышение уровней восстановленных форм глутатиона и тиолов на фоне снижения их окисленных форм. По митопротекторной активности на модели фокального инсульта Ронколейкин сопоставим с Тиотриазолином, а по ряду показателей - превосходит его.

Last decade a stable increase in morbidity is registered, pathogenesis of diseases involves basic or associated factor - afterhypoxic chain of pathophysiological changes in the tissue. In ischemia/hypoxia “cytokine cascade” is formed, in which ratio of cytokines, first of all interleukins, determines severity of afterhypoxic complication. Purpose of this study was determination of recombinant IL-2 (Ronkoleukin) influence on dynamics of afterhypoxic changes in tissues of rats’ brain with experimental focal stroke, mainly functional activity of mitochondria and thiol-disulfide system. Materials and methods. Mitoprotective activity of Ronkoleukin (0.01 mg/kg) comparing to Tiotriazoline (50 mg/kg) was studied on the model of experimental photo-induced thrombosis of brain in rats. In homogenate of brain in rats with experimental focal stroke in early and distant afterischemic periods after initiation with cyclosporine-A by spectrophotometry there was determined opening of mitochondrial pore and activity of thiol-disulfide system (levels of reduced forms of glutathions and thiols,activity of glutathionperoxidase and glutathionreductase). Results and discussion. On the model of focal stroke in rats afterischemic damage to brain tissue led to formation of dysfunction of mitochondria (by level of mitochondrial pore opening) and thiol-disulfide system - increase of level of glutathions and thiols on the background of reduction of their oxidized forms and activity of glutathionperoxidase and glutathionreductase. On Ronkoleukin administration background it was noted significant stabilization of mitochondria functional activity (by blocking mitochondrial pore opening) and state of thiol-disulfide system - normalization of activity of glutathionperoxidase and glutathionreductase, increase of levels of reduced forms of glutathions and thiols on the background of reduction of their oxidized forms. According to mitochondrial activity on the model of focal stroke, Ronkoleukin can be compared to Tiotriazoline and by some indices even better. Conclusions. Ronkoleukin has a mitoprotective effect in afterischemic damages that can be used as perspective therapy in complex therapy in treatment of afterischemic stroke and for effective protection of brain tissue.