Induction of oxidative stress in heart mitochondria in brain focal ischemia-reperfusion and protective effect of ecdysterone
Sharipov RR, Kotsiuruba AV, Kop"iak BS, Sahach VF.
O.O. Bogomoletz Institute of Physiology, National Academy of Sciences of Ukraine, Kyiv, Ukraine
DOI: https://doi.org/10.15407/fz60.03.011
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Abstract
Based on the fact that the acute phase of ischemic stroke is
accompanied by the development of heart damage, manifestations
of which are oxidative stress, morphological changes
in the myocardium, in the model of brain focal ischemia –
reperfusion, we investigated the oxidative stress in rat heart
mitochondria and possible mechanisms of cardioprotective
effect of ecdysterone. Under the conditions of brain focal ischemia
– reperfusion, there is an increase rate of the generation
of reactive oxygen species: superoxide (*O2
-) and hydroxyl
radicals (*OH), pools of stable hydrogen peroxide (H2O2), accumulate
products of lipid peroxidation (diene conjugates and
malonic dialdehyde), as a result of activation xanthine oxidase
(marker uric acid), lipooxygenase (marker leukotriene C4) and
cyclooxygenase (marker tromboksane B2) ways of *O2
-
generating.
In animals that received ecdysterone for 18 days, under
conditions of brain focal ischemia – reperfusion, the rate of
reactive oxygen species generation and the pools of lipid peroxidation
products were decreased, and the survival of animals
was increased. The obtained results support the development
of oxidative stress in heart mitochondria of rats, powerful antiradical
properties of ecdysterone, its cardioprotective effect,
in conditions of brain focal ischemia - reperfusion.
Keywords:
focal ischemia-reperfusion of the head brain, cerebrocardial syndrome, mitochondria of the heart, oxidative stress
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