Liraglutide, a glucagon-like peptide-1 analog, inhibits high glucose-induced oxidative stress and apoptosis in neonatal rat cardiomyocytes

• Published in: Experimental and therapeutic medicine Vol. 17; no. 5; pp. 3734 - 3740
• Main Authors: Zhang, Lihui, Li, Caige, Zhu, Qiuxiao, Li, Na, Zhou, Hong
• Format: Journal Article
• Language: English
• Published: Greece Spandidos Publications 01.05.2019; Spandidos Publications UK Ltd; D.A. Spandidos
• Subjects: Antidiabetics; Apoptosis; Atherosclerosis; Carbon dioxide; Cardiomyocytes; Care and treatment; Diabetes; Diabetes mellitus; Flow cytometry; Glucagon; Glucose; Health aspects; Heart cells; Hyperglycemia; Laboratory animals; Liraglutide; Lymphomas; Medical research; Mortality; Myocardial diseases; Newborn babies; Oxidative stress; Peptides; Prevention; Rodents; Studies; Superoxides; Testing; Tumors; Type 2 diabetes; United States > US; liraglutide; glucagon-like peptide-1 analog; high glucose; cardiomyocyte; apoptosis; diabetic cardiomyopathy; oxidative stress
• ISSN: 1792-0981; 1792-1015
• DOI: 10.3892/etm.2019.7388

Cardiomyocyte apoptosis serves an important role in diabetic cardiomyopathy. Liraglutide, a glucagon-like peptide-1 analog, has been indicated to exert a cardioprotective effect. However, the role of liraglutide on cardiomyocyte apoptosis in hyperglycemia is not fully understood. The aim of the current study was to assess whether liraglutide protects against high glucose (HG)-induced cardiomyocyte apoptosis . Sprague-Dawley neonatal rat cardiomyocytes were cultured in Dulbecco's modified Eagle's medium, supplemented with 5.5 or 25 mmol/l D-glucose or 5.5 mmol/l D-glucose + 19.5 mmol/l mannitol, in the presence or absence of liraglutide (10 or 100 nmol/l). Cell viability was assessed via an MTT assay and early apoptosis rates were assessed via flow cytometry. Superoxide dismutase (SOD) activity and malondialdehyde (MDA) content in cell supernatants were measured. Bcl-2 associated X (Bax), B-cell lymphoma-2 (Bcl-2) and cleaved/full caspase-3 protein levels were determined via western blotting. The results revealed that liraglutide effectively inhibited the HG-induced increase in early apoptosis and MDA content and markedly increased SOD activity. Furthermore, liraglutide markedly inhibited the HG-induced increase in Bax and cleaved caspase-3 protein expression, and upregulated the expression of Bcl-2. The present study demonstrated that liraglutide suppressed HG-induced oxidative stress and cardiomyocyte apoptosis. Thus, the anti-apoptotic actions of liraglutide may be attributable, in part, to the inhibition of Bax, the inhibition of caspase-3 activation and the upregualtion of Bcl-2.