Guanqun Ma1,2,3,4, Yingwu Liu1,2,3,4, Yu Wang1,2,3,4, Zhinan Wen1,2,3,4, Xin Li1,2,3,4, Hu Zhai1,2,3,4, Li Miao1,2,3,4, Jieying Luo1,2,3,4. 1. Department of Cardiology, The Third Central Hospital of Tianjin, Tianjin, China. 2. Tianjin Key Laboratory of Extracorporeal Life Support for Critical Diseases. 3. Artificial Cell Engineering Technology Research Center, Tianjin, China. 4. Tianjin Institute of Hepatobiliary Disease, Tianjin, China.
Abstract
Objective: Hyperglycemia-mediated cardiomyocyte damage is associated with inflammation and AMPK inactivation.Aim: The aim of our study is to explore the protective effects exerted by liraglutide on AMPK pathway and glucagon-like peptide 1 receptor in diabetic cardiomyopathy. Methods: Cardiomyocytes were treated with high-glucose stress and cardiomyocyte viability was determined via (3-(4,5-dimethylthiazol-2-yl)-2,5diphenyltetrazolium bromide assay. Besides, LDH release, immunofluorescence, and qPCR were used to verify the influence of liraglutide on hyperglycemia-treated cardiomyocytes. Results: Hyperglycemia treatment caused inflammation response and oxidative stress were significantly elevated in cardiomyocytes. This alteration could be reversed by liraglutide. Besides, cell viability was reduced whereas apoptosis was increased after exposure to high glucose treatment. However, liraglutide treatment could attenuate apoptosis and reverse cell viability in cardiomyocyte. Further, we found that AMPK pathway was also activated and glucagon-like peptide 1 receptor expression was increased in response to liraglutide treatment.Conclusions: Liraglutide could attenuate hyperglycemia-mediated cardiomyocyte damage through reversing AMPK pathway and upregulating glucagon-like peptide 1 receptor.
Objective: Hyperglycemia-mediated cardiomyocyte damage is associated with inflammation and AMPK inactivation.Aim: The aim of our study is to explore the protective effects exerted by liraglutide on AMPK pathway and glucagon-like peptide 1 receptor in diabetic cardiomyopathy. Methods: Cardiomyocytes were treated with high-glucose stress and cardiomyocyte viability was determined via (3-(4,5-dimethylthiazol-2-yl)-2,5diphenyltetrazolium bromide assay. Besides, LDH release, immunofluorescence, and qPCR were used to verify the influence of liraglutide on hyperglycemia-treated cardiomyocytes. Results: Hyperglycemia treatment caused inflammation response and oxidative stress were significantly elevated in cardiomyocytes. This alteration could be reversed by liraglutide. Besides, cell viability was reduced whereas apoptosis was increased after exposure to high glucose treatment. However, liraglutide treatment could attenuate apoptosis and reverse cell viability in cardiomyocyte. Further, we found that AMPK pathway was also activated and glucagon-like peptide 1 receptor expression was increased in response to liraglutide treatment.Conclusions: Liraglutide could attenuate hyperglycemia-mediated cardiomyocyte damage through reversing AMPK pathway and upregulating glucagon-like peptide 1 receptor.