Abstract
Objectives Diabetic cardiomyopathy (DC) has become one of the serious complications in diabetic cases. In this study, we aimed to explore the syringic acid (SYR) protective effect against diabetes-induced cardiac injury in experimental rats. Methods Rats were divided in control and streptozotocin-induced diabetic rats which were subdivided into diabetic controls, and three test groups (SYR at 25, 50, and 100 mg/kg) and the nondiabetic group received 100 mg/kg of SYR. All treatments were given SYR for 6 weeks. SYR effects on cardiac diagnostic markers, heart lipid peroxidation, protein carbonylation, antioxidant system, and changes of the heart mitochondrial mass and biogenesis were measured. Results Diabetes induction prompted CK-MB, LDH levels in serum, cardiac catalase, and superoxide dismutase activity, as well as cardiac TBARs and carbonylated protein. SYR administration (100 m/kg) attenuated CK-MB and LDH levels. Also, 50 and 100 mg/kg of SYR reduced cardiac TBARs and carbonylated protein in diabetic rats. These treatments did not show any effects on GSH content, mtDNA, and mitochondrial biogenesis indices (PGC1- α, NRF1, NRF2, and TFAM) in heart tissue. Conclusions SYR treatment showed protective effects on diabetic cardiomyopathy in rats by reducing lipid peroxidation and protein carbonylation. The possible mechanisms could be related to antioxidant activity of this phenolic acid. SYR might play a role of a protective factor in cardiac challenges in diabetes.
Highlights
Diabetic cardiomyopathy (DC) is one of the serious complications in diabetic patients
DC is responsible for almost 80% of mortality in patients suffering from diabetes [1]
Total RNA was extracted from cardiac tissues by using Trizol reagent (Pars Tous, Mashhad, Iran), and RNA was converted to cDNA based on the manufacturer’s protocol (Easy cDNA Synthesis Kit; Pars Tous, Iran)
Summary
Diabetic cardiomyopathy (DC) is one of the serious complications in diabetic patients. It is known by increasing some biomarkers such as low-density lipoprotein, glucose, glycated hemoglobin levels, and fibrotic markers insulin-like growth factor and transforming growth factor levels, accompanied by severe diastolic dysfunction. DC is responsible for almost 80% of mortality in patients suffering from diabetes [1]. Hyperglycemia, insulin resistance, and increased fatty acid metabolism are associated with DC progress. Some alterations in the cardiomyocytes are responsible for DCM. Ese alterations comprise apoptosis, diastolic dysfunction, inflammation, and imbalanced calcium homeostasis [1, 2]. As the heart is known as the high-metabolism-demanding organ, mitochondrial dysfunction is considerable in this organ [1]
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