Non-enzymatic modification of proteins and the level of galectin-3 in the rats with experimental myocardial ischemia

A. Shevtsova, V. Tkachenko, Yu. Kot
SI "Dnipropetrovsk Medical Academy of the Ministry of Health of Ukraine", Dnipro; SI "Dnipropetrovsk Medical Academy of the Ministry of Health of Ukraine", Dnipro; V. N. Karazin Kharkiv National University, Kharkiv

Abstract


The results of the determination of the products of oxidative modification, non-enzymatic protein glycation and galectin-3 under experimental
myocardial ischemia in rats with pituitrin-isoproterenol induced myocardial ischemia (PIIM), were presented in this work. Vasoconstriction and
increase of blood pressure under the action of pituitrin, together with the isoproterenol, which is a β-adrenoreceptor agonist, caused the condition
similar to acute myocardial infarction. The increase of the early (aldehyde phenylhydrazones, APH) and the late (ketone phenylhydrazones, KPH)
products of oxidative modification of proteins, as well as fluorescent advanced glycation end-products (AGE) were shown in blood of the rats with
PIIM. These changes were observed under normal content of glucose in the blood. At the same time, the presence of mono-, di, tri-, and tetrameric
forms of galectin-3, which is a scavenger of AGE, has been established in the blood of experimental animals. The levels of APH, KPH and AGE significantly
reduced under the impact of the antioxidants quercetin and 2-oxoglutarate, after the treatment with the AGE-inhibitor aminoguanidine,
tetracycline antibiotic doxycycline and eplerenone (selective antagonist of aldosterone receptors), although glucose concentration had a weak
tendency to increase. These changes were accompanied by the redistribution of mono- and oligomeric forms of galectin-3. Based on our results, it
was hypothesized that the removal of the products of oxidative modification of proteins and the inhibition of carbonyl-oxidative stress contribute to
the cardioprotective effect of the studied drugs.


Keywords


oxidative modification of proteins, glycation end-products, galectin 3, myocardial ischemia, cardioprotective drugs

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Received in the editorial: 26.09.2018

Received the revised version: 29.10.2018

Signed for press: 29.10.2018


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