Abstract: Objective To establish a stable, easily replicable, clinically relevant metabolic syndrome (MS) rat model of myocardial infarction, and explore the impact of MS on myocardial infarction. Methods Eighteen OLETF rats were used to establish the MS model，and 18 LETO rats were used as the control group. Rats were given high-fat diet and standard feed respectively. Model LETO rats and OLETF rats were randomly divided into sham operation group (sham group, MS-sham group) and myocardial infarction group (MI group, MS-MI group), 9 rats for each group. Echocardiography was used to measure left ventricular end-diastolic dimension (LVEDD), left ventricular end-systolic dimension (LVESD), left ventricular fraction shortening (LVFS), and left ventricular ejection fractions (LVEF). The levels of glutathione peroxidase (GSH-Px), total antioxidant capacity (T-AOC), myeloperoxidase (MPO) and malondialdehyde (MDA) in myocardial tissue were determined by ELISA. Western blot assay and RT-PCR were used to detect protein and mRNA levels of thioredoxin (TRX) and thioredoxin interacting protein (TXNIP) of myocardial tissue. Results There were effects of MS and MI on LVEDD, LVESD, LVFS and LVEF in rats (P＜0.05). The interaction between the two groups showed effects on LVEDD, LVFS and LVEF in rats (P＜0.05). MS and MI showed effects on GSH-Px, T-AOC, MPO, MDA, and levels of TRX and TXNIP protein and mRNA in rat myocardial tissues (P＜0.05). The interaction between the two groups showed effects on T-AOC, MDA and mRNA levels of TXNIP in rat myocardial tissues (P＜0.05). Conclusion This model is simple and practical. The disruption of TRX system stability may be one of the endogenous mechanisms, by which MS aggravates oxidative stress levels and decreases left ventricular function of myocardial tissue. The mechanism of MS affecting left ventricular function in MI still needs further investigation.

Key words: myocardial infarction, thioredoxins, disease models, animal, metabolic syndrome, left ventricular function； oxidative stress