RESUMEN
The objective of this study was to investigate the function and biological mechanisms of tricin in in-vivo damage to the myocardium produced by ischemia-reperfusion in LDLr -/- mice. The hypercholesterolemia animal model employed was male LDLr -/- mice. Coronary artery occlusion in mice resulted in the detection of oxidative stress and inflammatory pathology. In mice with coronary artery blockage, tricin reduced oxidative burden in the cardiac tissue and inflammatory mediators. Additionally, the ST segment of the animals receiving tricin was resumed. Tricine could dramatically lessen myocardial damage, according to pathological examination and triphenyltetrazolium chloride (TTC) staining. As a result of the research described above, the protective effects of tricin on myocardial injury have been explored, and the influence of inflammation and oxidative assaults in the ischemia-reperfusion injury (I/R) model of the heart has been demonstrated.