title: Cardioprotective effects of salidroside on myocardial ischemia-reperfusion injury in coronary artery occlusion-induced rats and Langendorff-perfused rat hearts.
abstract: OBJECTIVE
  The current study was designed to investigate the protective role of salisroside on rats through the study of energy metabolism homeostasis and inflammation both in ex vivo and in vivo.
  
  
  METHODS
  Energy metabolism homeostasis and inflammation injury were respectively assessed in global ischemia of isolated hearts and coronary artery ligated rats.
  
  
  RESULTS
  Excessive release of cardiac enzymes and pro-inflammatory cytokines was inhibited by salidroside in coronary artery occlusion-induced rats. ST segment was also restored with the treatment of salidroside. Triphenyltetrazolium chloride staining (TTC) staining and pathological analysis showed that salidroside could significantly alleviate myocardial injury in vivo. Accumulated data in ex vivo indicated that salidroside improved heart function recovery, which was reflected by enhanced myocardial contractility and coronary flow in isolated hearts. The contents of ATP and glycogen both in ex vivo and in vivo were restored by salidroside compared with those in the model group. Besides, the expressions of p-AMPK, PPAR-α and PGC-1α in rats and isolated hearts subjected to salidroside were significantly elevated, while the levels of p-NF-κBp65, p-IκBα, p-IKKα and p-IKKβ were dramatically reduced by salidroside.
  
  
  CONCLUSIONS
  The present study comprehensively elaborated the protective effects of salidroside on myocardial injury and demonstrated that AMPK/PGC-1α and AMPK/NF-κB signaling cascades were implicated in the myocardial ischemia-reperfusion injury (I/R) model.
authors.affiliation: Department of Physiology and Pharmacology, China Pharmaceutical University, Tongjiaxiang 24, Nanjing 210009, China.
authors.forename: Xiayun
authors.initials: X
authors.lastname: Chang
authors.affiliation: Department of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, Nanjing 210009, China.
authors.forename: Kai
authors.initials: K
authors.lastname: Zhang
authors.affiliation: Department of Physiology and Pharmacology, China Pharmaceutical University, Tongjiaxiang 24, Nanjing 210009, China.
authors.forename: Rui
authors.initials: R
authors.lastname: Zhou
authors.affiliation: Department of Physiology and Pharmacology, China Pharmaceutical University, Tongjiaxiang 24, Nanjing 210009, China.
authors.forename: Fen
authors.initials: F
authors.lastname: Luo
authors.affiliation: Department of Physiology and Pharmacology, China Pharmaceutical University, Tongjiaxiang 24, Nanjing 210009, China.
authors.forename: Lingpeng
authors.initials: L
authors.lastname: Zhu
authors.affiliation: Department of Physiology and Pharmacology, China Pharmaceutical University, Tongjiaxiang 24, Nanjing 210009, China.
authors.forename: Jin
authors.initials: J
authors.lastname: Gao
authors.affiliation: Department of Physiology and Pharmacology, China Pharmaceutical University, Tongjiaxiang 24, Nanjing 210009, China.
authors.forename: He
authors.initials: H
authors.lastname: He
authors.affiliation: Department of Physiology and Pharmacology, China Pharmaceutical University, Tongjiaxiang 24, Nanjing 210009, China.
authors.forename: Tingting
authors.initials: T
authors.lastname: Wei
authors.affiliation: Department of Physiology and Pharmacology, China Pharmaceutical University, Tongjiaxiang 24, Nanjing 210009, China. Electronic address: yantianhuabest@126.com.
authors.forename: Tianhua
authors.initials: T
authors.lastname: Yan
authors.affiliation: Department of Physiology and Pharmacology, China Pharmaceutical University, Tongjiaxiang 24, Nanjing 210009, China.
authors.forename: Chunhua
authors.initials: C
authors.lastname: Ma
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D002316:Cardiotonic Agents / Q000494:pharmacology*; D054059:Coronary Occlusion / Q000378:metabolism / Q000517:prevention & control*; D004734:Energy Metabolism / Q000187:drug effects; D005960:Glucosides / Q000494:pharmacology*; D006003:Glycogen / Q000378:metabolism; D066298:In Vitro Techniques; D000067268:Isolated Heart Preparation; D008297:Male; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000517:prevention & control*; D047493:PPAR alpha / Q000378:metabolism; D000071248:Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha / Q000378:metabolism; D010636:Phenols / Q000494:pharmacology*; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D002316:Cardiotonic Agents; D005960:Glucosides; D047493:PPAR alpha; D000071248:Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha; D010636:Phenols; D000255:Adenosine Triphosphate; D006003:Glycogen; C009172:rhodioloside
keywords: AMPK/NF-κB; AMPK/PGC-1α; Energy metabolism; Inflammation; Myocardial ischemia–reperfusion; Salidroside