Liraglutide preserves intracellular calcium handling in isolated murine myocytes exposed to oxidative stress

• Main Authors: S. Palee, S. C. Chattipakorn, N. Chattipakorn
• Format: Journal
• Published: 2018
• Subjects: Biochemistry, Genetics and Molecular Biology
• Online Access: https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85032960644&origin=inward; http://cmuir.cmu.ac.th/jspui/handle/6653943832/56812
• Institution: Chiang Mai University

© 2017 Institute of Physiology of the Czech Academy of Sciences, Prague, Czech Republic. In ischemic/reperfusion (I/R) injured hearts, severe oxidative stress occurs and is associated with intracellular calcium (Ca2+) overload. Glucagon-Like Peptide-1 (GLP-1) analogues have been shown to exert cardioprotection in I/R heart. However, there is little information regarding the effects of GLP-1 analogue on the intracellular Ca2+regulation in the presence of oxidative stress. Therefore, we investigated the effects of GLP-1 analogue, (liraglutide, 10 μM) applied before or after hydrogen peroxide (H2O2, 50 μM) treatment on intracellular Ca2+regulation in isolated cardiomyocytes. We hypothesized that liraglutide can attenuate intracellular Ca2+overload in cardiomyocytes under H2O2-induced cardiomyocyte injury. Cardiomyocytes were isolated from the hearts of male Wistar rats. Isolated cardiomyocytes were loaded with Fura-2/AM and fluorescence intensity was recorded. Intracellular Ca2+transient decay rate, intracellular Ca2+transient amplitude and intracellular diastolic Ca2+levels were recorded before and after treatment with liraglutide. In H2O2induced severe oxidative stressed cardiomyocytes (which mimic cardiac I/R) injury, liraglutide given prior to or after H2O2administration effectively increased both intracellular Ca2+transient amplitude and intracellular Ca2+transient decay rate, without altering the intracellular diastolic Ca2+level. Liraglutide attenuated intracellular Ca2+overload in H2O2-induced cardiomyocyte injury and may be responsible for cardioprotection during cardiac I/R injury by preserving physiological levels of calcium handling during the systolic and diastolic phases of myocyte activation.