Key result
Liraglutide and semaglutide improve post-ischemic myocardial recovery and reduce oxidative stress in metabolic syndrome rats.
Why the study?
Metabolic syndrome increases susceptibility to myocardial ischemia/reperfusion injury through metabolic disturbance, hypertension, and oxidative stress, necessitating evaluation of liraglutide and semaglutide effects.
Do liraglutide and semaglutide improve post-ischemic cardiac function, oxidative stress, and histomorphological changes in a rat model of metabolic syndrome?
Do liraglutide and semaglutide improve post-ischemic cardiac function, oxidative stress, and histomorphological changes in a rat model of metabolic syndrome?
Liraglutide and semaglutide exert significant cardioprotective and tissue-protective effects against ischemia/reperfusion injury in a rat model of metabolic syndrome.
Supports preclinical GLP-1RA cardioprotection in metabolic syndrome; leaves open translation to human ischemia/reperfusion injury.
BACKGROUND/OBJECTIVES: Metabolic syndrome (MetS) increases susceptibility to myocardial ischemia/reperfusion (I/R) injury through metabolic disturbance, hypertension, and oxidative stress. This study aimed to compare the effects of liraglutide and semaglutide on post-ischemic cardiac function, oxidative stress, and histomorphological changes in rats with MetS. METHODS: MetS was induced in male Wistar rats by a high-fat diet followed by low-dose streptozotocin. After confirmation of MetS, animals were treated with saline, liraglutide, or semaglutide for 6 weeks. Blood pressure, glycemia, oral glucose tolerance, and lipid profile were assessed during the protocol. In vivo cardiac function was evaluated by echocardiography, whereas ex vivo I/R injury was induced using the Langendorff technique. Cardiodynamic parameters, coronary flow, oxidative stress markers, and histological changes in the heart, liver, and pancreas were analyzed. RESULTS: Both liraglutide and semaglutide improved the cardiometabolic profile of MetS rats, with semaglutide showing a more evident effect on body weight control. In the Langendorff model, both treatments improved post-ischemic recovery of myocardial contractility and relaxation during reperfusion. Treated animals also showed a more favorable oxidative stress profile, particularly lower superoxide anion levels and enhanced antioxidant defense. Histologically, both agents attenuated myocardial hypertrophy and collagen deposition, improved hepatic architecture by reducing inflammatory changes, and preserved pancreatic structure with less lipid accumulation and tissue injury. CONCLUSIONS: Liraglutide and semaglutide exerted significant cardioprotective and tissue-protective effects in experimental MetS complicated by myocardial I/R injury. These findings support their potential in limiting post-ischemic cardiac dysfunction and multiorgan damage in metabolically compromised conditions.
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Ravić et al. (2026) studied Metabolic syndrome and myocardial ischemia/reperfusion injury (n=30). Liraglutide and Semaglutide vs. Saline (0.9% NaCl) was evaluated on Post-ischemic cardiac function and oxidative stress. Liraglutide and semaglutide significantly improved post-ischemic recovery of myocardial contractility and relaxation, and reduced oxidative stress in an experimental rat model of metabolic syndrome.
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