title: Sophocarpine administration preserves myocardial function from ischemia-reperfusion in rats via NF-κB inactivation.
abstract: BACKGROUND
  Sophora alopecuroides L. (the clinical usefulness of compound Kudouzi injection) has been used mainly for the treatment of fever, inflammation, edema and pain. Sophocarpine, a tetracyclic quinolizidine alkaloid, is one of the most abundant active ingredients in Sophora alopecuroides L. Sophocarpine injection (called the Kangke injection) has been demonstrated to have significant antivirus effects against coxsackievirus B3 and therapeutic effects for viral myocarditis in clinical.
  
  
  OBJECTIVE
  The present study was to evaluate the protective effect of sophocarpine on the inhibition of NF-kappaB (NF-κB) and effect on inflammatory markers during myocardial ischemia-reperfusion (I/R) injury in rat.
  
  
  METHODS
  Myocardial I/R injury was induced by the occlusion of left anterior descending coronary artery for 30 min followed by reperfusion for 2 h. 2 h after reperfusion was established, the hemodynamics and infarct size were examined. Blood samples were collected for biochemical analysis. Expression of NF-κB and mitogen-activated protein kinases (MAPKs) in ischemic myocardial tissue were assayed by western blot.
  
  
  RESULTS
  Administration of sophocarpine significantly improved cardiac function and reduced infarct size in I/R rat heart in vivo. Furthermore, sophocarpine ameliorated the contents of inflammatory mediators (tumor necrosis factor-alpha, TNF-α; interleukin-6, IL-6; IL-10), neutrophil infiltration and myeloperoxidase (MPO) activity. Interestingly, sophocarpine also significantly inhibited translocation of NF-κB, which was associated with attenuated phosphorylations of p38 and c-Jun NH2-terminal protein kinase (JNK).
  
  
  CONCLUSIONS
  Inflammatory mediators, infiltration of neutrophil, and MPO were ameliorated via down-regulation of JNK and p38, and inactivation of NF-κB. This might be one of the important mechanisms of sophocarpine that protected myocardial injury from I/R.
authors: School of Pharmacy, Yantai University, Yantai, 32 Qingquan Road Laishan District, Yantai, Shandong 264005, PR China.
authors: Chunmei
authors: C
authors: Li
authors: Yonglin
authors: Y
authors: Gao
authors: Jingwei
authors: J
authors: Tian
authors: Jingyu
authors: J
authors: Shen
authors: Yanli
authors: Y
authors: Xing
authors: Zhifeng
authors: Z
authors: Liu
mesh_terms: D000470:Alkaloids / Q000302:isolation & purification / Q000494:pharmacology / Q000627:therapeutic use*; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000302:isolation & purification / Q000494:pharmacology / Q000627:therapeutic use*; D001692:Biological Transport / Q000187:drug effects; D054059:Coronary Occlusion; D006321:Heart / Q000187:drug effects / Q000503:physiopathology; D018836:Inflammation Mediators / Q000378:metabolism; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism; D009203:Myocardial Infarction / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D016328:NF-kappa B / Q000037:antagonists & inhibitors*; D009504:Neutrophils / Q000378:metabolism; D009195:Peroxidase / Q000378:metabolism; D008517:Phytotherapy; D010936:Plant Extracts / Q000737:chemistry / Q000494:pharmacology / Q000627:therapeutic use; D051381:Rats; D017207:Rats, Sprague-Dawley; D012639:Seeds; D029909:Sophora / Q000737:chemistry*; D000093842:Matrines
chemical_list: D000470:Alkaloids; D000893:Anti-Inflammatory Agents; D018836:Inflammation Mediators; D020928:Mitogen-Activated Protein Kinases; D016328:NF-kappa B; D009195:Peroxidase; D010936:Plant Extracts; C035933:sophocarpine; D000093842:Matrines