title: Caffeic acid ethanolamide prevents cardiac dysfunction through sirtuin dependent cardiac bioenergetics preservation.
abstract: BACKGROUND
  Cardiac oxidative stress, bioenergetics and catecholamine play major roles in heart failure progression. However, the relationships between these three dominant heart failure factors are not fully elucidated. Caffeic acid ethanolamide (CAEA), a synthesized derivative from caffeic acid that exerted antioxidative properties, was thus applied in this study to explore its effects on the pathogenesis of heart failure.
  
  
  RESULTS
  In vitro studies in HL-1 cells exposed to isoproterenol showed an increase in cellular and mitochondria oxidative stress. Two-week isoproterenol injections into mice resulted in ventricular hypertrophy, myocardial fibrosis, elevated lipid peroxidation, cardiac adenosine triphosphate and left ventricular ejection fraction decline, suggesting oxidative stress and bioenergetics changes in catecholamine-induced heart failure. CAEA restored oxygen consumption rates and adenosine triphosphate contents. In addition, CAEA alleviated isoproterenol-induced cardiac remodeling, cardiac oxidative stress, cardiac bioenergetics and function insufficiency in mice. CAEA treatment recovered sirtuin 1 and sirtuin 3 activity, and attenuated the changes of proteins, including manganese superoxide dismutase and hypoxia-inducible factor 1-α, which are the most likely mechanisms responsible for the alleviation of isoproterenol-caused cardiac injury
  
  
  CONCLUSIONS
  CAEA prevents catecholamine-induced cardiac damage and is therefore a possible new therapeutic approach for preventing heart failure progression.
authors.affiliation: Institute of Pharmacology, College of Medicine, National Taiwan University, No.1, Sec.1, Jen-Ai Road, Taipei, 10051, Taiwan.|Division of Pulmonary and Critical Care Medicine, Mackay Memorial Hospital, Taipei, Taiwan.|Mackay Junior College of Medicine, Nursing, and Management, Taipei, Taiwan.
authors.forename: Shih-Yi
authors.initials: SY
authors.lastname: Lee
authors.affiliation: Institute of Pharmacology, College of Medicine, National Taiwan University, No.1, Sec.1, Jen-Ai Road, Taipei, 10051, Taiwan.
authors.forename: Hui-Chun
authors.initials: HC
authors.lastname: Ku
authors.affiliation: Department of Chinese Pharmaceutical Sciences and Chinese Medicine Resources, China Medical University, Taichung, Taiwan.|Department of Biotechnology, Asia University, Taichung, Taiwan.
authors.forename: Yueh-Hsiung
authors.initials: YH
authors.lastname: Kuo
authors.affiliation: Institute of Pharmacology, College of Medicine, National Taiwan University, No.1, Sec.1, Jen-Ai Road, Taipei, 10051, Taiwan.
authors.forename: Kai-Chien
authors.initials: KC
authors.lastname: Yang
authors.affiliation: Department of Chinese Pharmaceutical Sciences and Chinese Medicine Resources, China Medical University, Taichung, Taiwan.
authors.forename: Ping-Chen
authors.initials: PC
authors.lastname: Tu
authors.affiliation: Department of Chemistry, National Taiwan University, Taipei, Taiwan.
authors.forename: His-Lin
authors.initials: HL
authors.lastname: Chiu
authors.affiliation: Institute of Pharmacology, College of Medicine, National Taiwan University, No.1, Sec.1, Jen-Ai Road, Taipei, 10051, Taiwan. mingja@ntu.edu.tw.
authors.forename: Ming-Jai
authors.initials: MJ
authors.lastname: Su
mesh_terms: D000818:Animals; D002109:Caffeic Acids / Q000138:chemical synthesis / Q000737:chemistry / Q000494:pharmacology; D002460:Cell Line; D004734:Energy Metabolism / Q000187:drug effects*; D006333:Heart Failure / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D006801:Humans; D015227:Lipid Peroxidation / Q000187:drug effects*; D008297:Male; D051379:Mice; D032383:Myocytes, Cardiac / Q000378:metabolism* / Q000473:pathology; D037761:Sirtuins / Q000096:biosynthesis*
chemical_list: D002109:Caffeic Acids; D037761:Sirtuins