Protective effect of uridine on metabolic processes in rat myocardum during its ischemia/reperfusion damage

   
Bulion V.V.1, Selina E.N.1, Krylova I.B.1

1. Institute of Experimental Medicine, St. Petersburg, Russia
Section: Experimental Study
DOI: 10.18097/PBMC20196505398      PubMed Id: 31666412
Year: 2019  Volume: 65  Issue: 5  Pages: 398-402
The experimental study of the cardioprotective effect of uridine, the metabolic precursor of the endogenous activator of mitochondrial ATP-dependent K+-channels (mitoKATP-channels), was performed using the model of myocardial ischemia/reperfusion (I/RP) in rats. Ischemia for 30 min followed by reperfusion for 120 min resulted in a significant decrease in ATP and phosphocreatine (PC) content, intensification of lipid peroxidation (LPO), and inhibition of the antioxidant system (AOS) in cardiomyocytes. Uridine in a dose of 30 mg/kg, administered intravenously prior to reperfusion, had a protective effect on myocardial metabolism in the I/RP zone. It prevented the decrease of ATP and PC, limited the LPO processes, evaluated by the content of lipid hydroperoxides and conjugated dienes, and improved the AOS state by, preventing the decrease of superoxide dismutase (SOD) activity and increasing the content of reduced glutathione (GSH). The mitoKATP-channel blocker 5-hydroxydecanoate (5-HD, 5 mg/kg) eliminated the ability of uridine to maintain the ATP level and to exhibit its positive effect on the intensity of the LPO and activity of AOS. The obtained data allow us to conclude that activation of mitoKATP-channels play an important role in the mechanism of the cardioprotective effect of uridine in I/RP damage of myocardium.
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Keywords: uridine, ischemia/reperfusion, myocardium, mitochondrial ATP-dependent K+-channels
Citation:

Bulion, V. V., Selina, E. N., Krylova, I. B. (2019). Protective effect of uridine on metabolic processes in rat myocardum during its ischemia/reperfusion damage. Biomeditsinskaya khimiya, 65(5), 398-402.
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