Abstract
Based on the fact that the acute phase of ischemic stroke is accompanied by the development of cerebrocardial syndrome, oxidative stress in the rat heart mitochondria and possible mechanisms of cardioprotective action of ecdysterone were examined using the model of focal cerebral ischemia-reperfusion. When focal cerebral ischemia-reperfusion, the rate of reactive oxygen species generation, namely superoxide (. O2− ) and hydroxyl radical (. OH), pools of stable hydrogen peroxide (H2O2) increases, and products of lipid peroxidation (diene conjugates and malonic dialdehyde) are accumulated due to the activation of xanthine oxidase (uric acid as a marker), lipoxygenase (leukotriene C4 as marker), and cyclooxygenase (thromboxane B2 as a marker) ways of·O2- generating. In animals treated with ecdysterone for 18 days, the rate of reactive oxygen species generation decreases, pools of lipid peroxidation products are reduced, the ways of·O2-generating are inhibited, mortality of animals decreases. The results obtained confirm the development of oxidative stress in the rat heart mitochondria, strong antiradical properties of ecdysterone, cardioprotective effect of the latter under focal cerebral ischemia-reperfusion.
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