High-density lipoprotein ameliorates palmitic acid-induced lipotoxicity and oxidative dysfunction in H9c2 cardiomyoblast cells via ROS suppression

• Published in: Nutrition & metabolism Vol. 16; no. 1; p. 36
• Main Authors: Wu, Kuen-Ming, Hsu, Yuan-Man, Ying, Mei-Chin, Tsai, Fuu-Jen, Tsai, Chang-Hai, Chung, Jing-Gung, Yang, Jai-Sing, Tang, Chih-Hsin, Cheng, Li-Yi, Su, Po-Hua, Viswanadha, Vijaya Padma, Kuo, Wei-Wen, Huang, Chih-Yang
• Format: Journal Article
• Language: English
• Published: England BioMed Central Ltd 28.05.2019; BioMed Central; BMC
• Subjects: Angina pectoris; anti-inflammatory activity; Apoptosis; Atherosclerosis; Cardiomyoblast; Cardiomyocytes; Cardiomyopathy; Cardiovascular disease; Care and treatment; Caspase; Caspase-3; Cell death; Cell proliferation; Cholesterol; Congestive heart failure; Cytochrome c; Cytosol; Development and progression; Diabetes; Diabetes mellitus; dose response; Fatty acids; Flow cytometry; Heart failure; High density lipoprotein; Hyperlipidemia; Inflammation; Insulin resistance; Ischemia; Kinases; Lipids; Lipoproteins; Lipotoxicity; Membrane potential; Metabolic syndrome; Mitochondria; mitochondrial membrane; mitogen-activated protein kinase; NF-κB protein; Obesity; Oxidative stress; Palmitic acid; Phosphorylation; Proteins; Risk factors; ROS; Transcription factors; Tumor necrosis factor-TNF; Cardiomyoblast; High-density lipoprotein; Lipotoxicity; Palmitic acid; ROS
• ISSN: 1743-7075; 1743-7075
• DOI: 10.1186/s12986-019-0356-5

High levels circulating saturated fatty acids are associated with diabetes, obesity and hyperlipidemia. In heart, the accumulation of saturated fatty acids has been determined to play a role in the development of heart failure and diabetic cardiomyopathy. High-density lipoprotein (HDL) has been reported to possess key atheroprotective biological properties, including cellular cholesterol efflux capacity, anti-oxidative and anti-inflammatory activities. However, the underlying mechanisms are still largely unknown. Therefore, the aim of the present study is to test whether HDL could protect palmitic acid (PA)-induced cardiomyocyte injury and explore the possible mechanisms. H9c2 cells were pretreated with HDL (50-100 μg/ml) for 2 h followed by PA (0.5 mM) for indicated time period. Our results showed that HDL inhibited PA-induced cell death in a dose-dependent manner. Moreover, HDL rescued PA-induced ROS generation and the phosphorylation of JNK which in turn activated NF-κB-mediated inflammatory proteins expressions. We also found that PA impaired the balance of BCL family proteins, destabilized mitochondrial membrane potential, and triggered subsequent cytochrome c release into the cytosol and activation of caspase 3. These detrimental effects were ameliorated by HDL treatment. PA-induced ROS accumulation and results in cardiomyocyte apoptosis and inflammation. However, HDL attenuated PA-induced lipotoxicity and oxidative dysfunction via ROS suppression. These results may provide insight into a possible molecular mechanism underlying HDL suppression of the free fatty acid-induced cardiomyocyte apoptosis.