AI Summary & Key Takeaways
AI InsightPostC and melatonin may regulate energy metabolism and inflammatory mediators and protect mitochondria by affecting theUCP3, irisin, and NFkB levels. (Anatol J Cardiol 2020; 23: 19-27)
📌 3 Key Takeaways
Özet
Objective: Protective effects of ischemic postconditioning (PostC) decrease/disappear with age and chronic heart diseases. Similarly, low serummelatonin levels have been reported in the same risk groups. The aims of this study were to investigate the effects of melatonin on the protection of PostC in ischemia–reperfusion (I/R)-induced infarct size and roles of uncoupling protein (UCP) 3, irisin, and nuclear factor kappa B (NFkB)levels.Methods: Rats were pinealectomized (Px) or sham operated (non-Px) 2 months before the I/R studies. The left main coronary artery was occluded for 30 min followed by 120 min reperfusion. PostC was induced with three cycles of R/I (10 s each) after ischemia.Results: The infarct size was found to be significantly higher in Px rats (54.68±1.5%) than in the control group (35.1±2.5%). PostC and melatoninadministrations to non-Px rats significantly reduced the infarct size. On the other hand, PostC did not create a significant effect in Px rats, butprotection was provided when PostC was co-administrated with melatonin. While significant decreases were detected in the UCP3 levels, irisinand NFkB levels increased with I/R and Px. Treatment with PostC and melatonin in non-Px groups and their co-administration in Px groups werefound to return all the genes close to normal levels.Conclusion: The physiological and pharmacological concentrations of melatonin may play a role in the protection of PostC. In cases when physiological melatonin is reduced, such as aging and heart diseases, this protection may decrease, and this effect may be restored by melatoninreplacement. PostC and melatonin may regulate energy metabolism and inflammatory mediators and protect mitochondria by affecting theUCP3, irisin, and NFkB levels. (Anatol J Cardiol 2020; 23: 19-27)