Advanced glycation end products in isoproterenol-induced acute myocardial infarction

Abstract

Background. Isoproterenol is a synthetic catecholamine that can produce diffuse myocardial necrosis at high doses. Advanced glycation end products (AGEs) are involved in the development and progression of cardiovascular disease, including acute coronary syndrome. The purpose of the study was to determine the changes of serum and tissue AGE content in isoproterenol-induced acute myocardial infarction and to assess their informational character in the early diagnosis, risk stratification and prognosis of disease.
 Methods. Forty adult male rats were divided into 5 groups: sham (L1=11), control 0.9% NaCl (L2=11), and with experimental myocardial infarction (L3=6, L4=6; L5=6), induced by the subcutaneous injection of Isoproterenol Hydrochloride solution 100 mg/kg, and sacrificed over 6 hours, 24 hours and 7 days post infarction. The results were presented by median and interquartile range. The groups were compared using Kruskal-Wallis and Mann-Whitney nonparametric tests, and the Spearman correlation coefficient was calculated (SPSS 23.0).
 Results. A decrease of AGE serum levels in L3 were identified, followed by a significant increase in L4, the trend maintained in L5, which significantly exceeded the values in sham and control groups. In the homogenate, AGEs presented an elevation in L3, with a relevant decrease in L4, and an inconsistent increase in L5 compared to sham and control groups.
 Conclusion. The collected data suggest the utility of AGE assessment in early diagnosis and risk stratification in acute myocardial infarction.

Visnagin prevents isoproterenol‐induced myocardial injury by attenuating oxidative stress and inflammation and upregulating Nrf2 signaling in rats

“…Isoproterenol (ISO) is a synthetic catecholamine and β‐adrenergic agonist that is beneficial in regulating heart function by exerting positive chronotropic and inotropic effects on the myocardium; however, it can produce infarct‐like myocardial lesions at high doses. [ 5,6 ] The pathological changes observed in rodent ISO‐induced MI resemble those observed in human MI. Therefore, this experimental model is widely used to assess the cardioprotective effects of various compounds.…”

Cardioprotective Effect of Taxifolin against Isoproterenol-Induced Cardiac Injury through Decreasing Oxidative Stress, Inflammation, and Cell Death, and Activating Nrf2/HO-1 in Mice

“…Despite the broad availability of therapeutic options, MI is still a leading cause of morbidity and death globally; hence, new therapeutic tools for the prevention/treatment of MI are needed. Isoproterenol (ISO) is a common treatment of bradycardia and heart block by acting as a non-selective beta agonist; however, it can lead to functional and structural changes in the myocardium resembling pathological changes observed in acute MI when given at high doses [ 5 , 6 ]. The molecular mechanism by which ISO-induced myocardial injury is complex and multifactorial, with oxidative stress assumed to be the main fundamental mechanism producing pathologic complications involved in ISO cardiotoxicity [ 6 , 7 ].…”

Accumulation of Advanced Glycation End-Products in the Body and Dietary Habits

“…AGE affects the cells of osteoblasts’ outer membrane, which leads to calcification in glycated sites [ 42 ]. In fact, the formation of calcium deposits in the atherosclerotic plaque area occurs in the advanced stages of atherosclerosis and affects the occurrence of myocardial infarction [ 43 , 44 ]. The accumulation of AGE in the body affects the success rate of coronary revascularization in individuals with diabetes [ 45 ].…”