Abstract 70: Characterization of Advanced Glycation End Products in a Myocardial Infarction Animal Model

Abstract

Advanced glycation end products (AGE) are molecules produced by oxidative and inflammatory metabolism. Studies have shown that increased AGE levels worse the prognosis of the cardiovascular diseases. However, there is no characterization of AGE generation in a representative animal model of myocardial infarction (MI). Thus, our goal was to characterize the AGE formation in plasma and cardiac tissue in an animal model of MI. Male Wistar rats (3 month-old) were divided in 2 groups: Sham (n = 15) and MI (n = 14) and followed by 12 week. MI was induced by left anterior descending coronary artery (LAD) permanent ligation and the animals were stratified in 2 groups according to ejection fraction (EF) median at 2 days post-MI. MI induced 47% and 29% increase in heart weight/final body weight ratio in MIlowEF MIhighEF group, respectively. There was no significant difference among the groups in the plasma levels of reactive free amines, fluorescents AGE, Nε-(Carboxymethyl)lysine (CML) and Nε-(Carboxyethyl)lysine (CEL) in a 12-week follow-up. However, a significant decrease in the levels of yellowish-brown colored AGEs was revealed in MIlowEF group when compared to Sham. In the cardiac tissue homogenate there was no difference in the amounts of reactive free amines and carbonyl protein among the groups. Our results suggest that a widely employed animal model of MI partially agrees with the human manifestation of the ischemic heart disease concerning the AGEs metabolism. Thus, its use must be employed with caution when studying AGEs signaling or anti-AGE drugs.