High-density lipoprotein ameliorates palmitic acid-induced lipotoxicity and oxidative dysfunction in H9c2 cardiomyoblast cells via ROS suppression
| Autor: | Chih-Hsin Tang, Chang Hai Tsai, Vijaya Padma Viswanadha, Kuen-Ming Wu, Wei Wen Kuo, Po-Hua Su, Li-Yi Cheng, Fuu Jen Tsai, Mei-Chin Ying, Chih Yang Huang, Jing Gung Chung, Jai Sing Yang, Yuan-Man Hsu |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2019 |
| Předmět: |
medicine.medical_specialty
030309 nutrition & dietetics Endocrinology Diabetes and Metabolism Cardiomyoblast Medicine (miscellaneous) lcsh:TX341-641 Caspase 3 Oxidative phosphorylation 03 medical and health sciences chemistry.chemical_compound High-density lipoprotein Palmitic acid Internal medicine Diabetic cardiomyopathy Hyperlipidemia medicine lcsh:RC620-627 0303 health sciences Nutrition and Dietetics biology Chemistry Cytochrome c Research ROS medicine.disease lcsh:Nutritional diseases. Deficiency diseases Endocrinology Lipotoxicity biology.protein lcsh:Nutrition. Foods and food supply Lipoprotein |
| Zdroj: | Nutrition & Metabolism Nutrition & Metabolism, Vol 16, Iss 1, Pp 1-13 (2019) |
| ISSN: | 1743-7075 |
| Popis: | Background 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. Results 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 BCL2 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. Conclusion 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. |
| Databáze: | OpenAIRE |
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