title: [Induction of oxidative stress in heart mitochondria in brain focal ischemia-reperfusion and protective effect of ecdysterone].
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 ofecdysterone, its cardioprotective effect, in conditions of brain focal ischemia-reperfusion.
authors.forename: R R
authors.initials: RR
authors.lastname: Sharipov
authors.forename: A V
authors.initials: AV
authors.lastname: Kotsiuruba
authors.forename: B S
authors.initials: BS
authors.lastname: Kop"iak
authors.forename: V F
authors.initials: VF
authors.lastname: Sahach
mesh_terms: D000818:Animals; D002545:Brain Ischemia / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D002316:Cardiotonic Agents / Q000494:pharmacology*; D004441:Ecdysterone / Q000494:pharmacology*; D006321:Heart / Q000187:drug effects; D006861:Hydrogen Peroxide / Q000037:antagonists & inhibitors / Q000378:metabolism; D017665:Hydroxyl Radical / Q000037:antagonists & inhibitors / Q000378:metabolism; D007447:Invertebrate Hormones / Q000494:pharmacology*; D015227:Lipid Peroxidation / Q000187:drug effects; D008084:Lipoxygenase / Q000378:metabolism; D008315:Malondialdehyde / Q000037:antagonists & inhibitors / Q000378:metabolism; D008929:Mitochondria, Heart / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D018384:Oxidative Stress; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D013481:Superoxides / Q000037:antagonists & inhibitors / Q000378:metabolism; D016019:Survival Analysis; D014969:Xanthine Oxidase / Q000037:antagonists & inhibitors / Q000378:metabolism
chemical_list: D002316:Cardiotonic Agents; D007447:Invertebrate Hormones; D013481:Superoxides; D017665:Hydroxyl Radical; D008315:Malondialdehyde; D004441:Ecdysterone; D006861:Hydrogen Peroxide; D008084:Lipoxygenase; D011451:Prostaglandin-Endoperoxide Synthases; D014969:Xanthine Oxidase