%0 Journal Article %T The effects of ginsenoside Rb1 on fatty acid β-oxidation, mediated by AMPK, in the failing heart %J Iranian Journal of Basic Medical Sciences %I Mashhad University of Medical Sciences %Z 2008-3866 %A Kong, Hong-liang %A Hou, Ai-jie %A Liu, Ning-ning %A Chen, Bo-han %A Huang, Hua-ting %A Dai, Sheng-nan %D 2018 %\ 07/01/2018 %V 21 %N 7 %P 731-737 %! The effects of ginsenoside Rb1 on fatty acid β-oxidation, mediated by AMPK, in the failing heart %K AMP-activated protein kinase %K Carnitine palmitoyl-transferase 1 %K Ginsenosides-Rbl %K heart failure %K L-carnitine %K Long-chain acyl-CoA synthetase %K Malonyl-CoA %K Medium-chain acyl-CoA dehydrogenase %R 10.22038/ijbms.2018.24002.6016 %X Objective(s): This study intended to investigate the effects of Ginsenoside-Rbl (Gs-Rbl) on fatty acid β-oxidation (FAO) in rat failing heart and to identify potential mechanisms of Gs-Rbl improving heart failure (HF) by FAO pathway dependent on AMP-activated protein kinase (AMPK). Materials and Methods: Rats with chronic HF, induced by adriamycin (Adr), were randomly grouped into 7 groups. Gs-Rb1, adenine 9-β-D-arabinofuranoside (Ara A, specific AMPK inhibitor), and 5'-aminoimidazole-4-carboxamide riboside (Aicar, specific AMPK activator) were administered to rats with HF, singly and/or combinedly. Myocardial high-energy phosphate (such as phosphocreatine, ADP, and ATP), free L-Carnitine, malonyl-CoA, and the activity of FAO-related enzymes in left ventricle from different groups were measured by using the corresponding molecular biological techniques. Results: Gs-Rb1 improved HF significantly, accompanied by a significant increase in phosphocreatine (PCr), ADP, ATP, PCr/ATP ratio, free carnitine, malonyl-CoA, mRNA, activity of carnitine palmitoyltransferase (Cpt), medium-chain Acyl-CoA Dehydrogenase (MCAD) and long-chain acyl-CoA Synthetase (ACSL) and a significant decrease of the ADP/ATP ratio in the left ventricular myocardium. However, all those effects were almost abolished by Ara A and were not further improved by Aicar. Conclusion: Taken together, it suggests that Gs-Rb1 may modulate cardiac metabolic remodeling by improving myocardial fatty acid β-oxidation in failing heart. In addition, the effects of Gs-Rb1 may be mediated via activating AMPK. %U https://ijbms.mums.ac.ir/article_10799_738310e75df0cd60895cd71bc8cb5bd1.pdf