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Scientists from the Institute of Theoretical and Experimental Biophysics of the Russian Academy of Sciences and the Institute of Experimental Medicine used uridine (pyrimidine nucleoside, an RNA component) to protect rat myocardial tissue from ischemic and reperfusion damage and identified a possible mechanism of its protective action.

Cardiovascular diseases have been the main cause of death in most countries of the world for two centuries, so the search for fundamentally new ways to prevent them is one of the most urgent medical tasks. Currently, it has been established in many laboratories around the world that pharmacological activators of the mitochondrial ATP-dependent potassium channel (MITOC-ATP) have a pronounced therapeutic effect in pathologies associated with the development of oxidative stress, such as cardiovascular and neurodegenerative diseases.

Earlier, scientists from Pushchino under the guidance of Doctor of Biological Sciences, Professor, Head of the Laboratory of Mitochondrial Transport of the ITEB RAS, Honored Scientist of the Russian Federation Galina Dmitrievna Mironova discovered a metabolic activator of the potassium channel of mitochondria (MITOC-ATP) - 5-uridine diphosphate (UDP) and showed that its precursor uridine, penetrating into cells, effectively protects tissues from oxidative stress.

In the development of this approach, the researchers conducted a series of experiments to study the effect of uridine on myocardial tissue in violation of blood flow: its termination — ischemia, and subsequent abrupt recovery - reperfusion. It is known that when restoring blood circulation in damaged tissues, oxygen and accumulated toxins (products of peroxidation, calcium) entering in large quantities can further enhance myocardial damage.

"The work was carried out on two experimental models: acute ischemia and ischemia/reperfusion of the heart, created in rats. In both models, uridine treatment prevented disturbances in the energy supply of cells and the activity of the antioxidant system. This led to a decrease in the necrosis zone and restoration of the heart rhythm. To prove the role of the potassium channel in the cardioprotective effect of uridine, an inhibitory analysis was performed using 5-hydroxydecanoate as a blocker of this channel. We have shown for the first time that intravenously administered uridine is excreted from the blood faster in hypoxia than in normoxia, and the level of the potassium channel activator - UDP - in the myocardium increases significantly after uridine administration. This can enhance the work of potassium channels and contribute to the activation of intracellular defense mechanisms in the treatment of cardiac pathologies with uridine," said Natalia Belosludtseva, one of the authors of the article, Candidate of Biological Sciences, leading researcher at the Laboratory of Mitochondrial Transport at ITEB RAS.

The results indicate that the use of uridine may be a potentially effective approach to the treatment of myocardial infarction and other cardiovascular pathologies. The advantage of this line of research is that it is proposed to use not synthetic mitoC-ATP activators, which has recently been widely practiced abroad, but a metabolic (natural) activator, which, according to the authors, is much more promising in terms of its further use as a medicinal compound.

The article was published in the journal Scientific Reports
PHOTO: Uridine molecule Model © Jynto/ Discovery Studio Visualizer

Source: polit.ru, sci-dig.ru