title: Erianin induces a JNK/SAPK-dependent metabolic inhibition in human umbilical vein endothelial cells.
abstract: BACKGROUND
  Erianin is a natural product derived from Dendrobium chrysotoxum, with promising antitumor activity.
  
  
  METHODS
  To evaluate the metabolic effect of erianin, a cytosensor assay for acidification rate, MTT assay, measurement of lactate, glucose and ATP were performed in human umbilical vein endothelial cells (HUVECs) exposed to 1-100 nM erianin. JNK/SAPK activity was detected by Western blot.
  
  
  RESULTS
  Twelve- or 24- hour incubation with erianin induced a dose-dependent metabolic inhibition, as indicated by reduced acidification rate and cell viability, with an endothelium-selectivity. Erianin caused decreases in lactate production, glucose consumption and intracellular ATP level. Pretreatment with the JNK/SAPK inhibitor SP600125 significantly abolished these inhibitory responses, and especially restored the erianin-induced decreases in ATP and the erianin-induced phosphorylation of JNK/SAPK with dose- and time- dependence.
  
  
  CONCLUSIONS
  Erianin inhibited endothelial metabolism in a JNK/SAPK-dependent manner. This mechanism may be involved in the potential antitumnor and antiangiogenic actions of erianin.
authors.affiliation: Department of Pharmacognosy, China Pharmaceutical University, Nanjing 210038 , P.R. China.
authors.forename: Yanqing
authors.initials: Y
authors.lastname: Gong
authors.forename: Yi
authors.initials: Y
authors.lastname: Fan
authors.forename: Lei
authors.initials: L
authors.lastname: Liu
authors.forename: Dazheng
authors.initials: D
authors.lastname: Wu
authors.forename: Zongliang
authors.initials: Z
authors.lastname: Chang
authors.forename: Zhengtao
authors.initials: Z
authors.lastname: Wang
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D020533:Angiogenesis Inhibitors / Q000494:pharmacology*; D000873:Anthracenes / Q000494:pharmacology; D001632:Bibenzyls / Q000494:pharmacology*; D015374:Biosensing Techniques; D002478:Cells, Cultured; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D005562:Formazans / Q000378:metabolism; D005947:Glucose / Q000378:metabolism; D006801:Humans; D006863:Hydrogen-Ion Concentration; D019344:Lactic Acid / Q000378:metabolism; D048057:Mitogen-Activated Protein Kinase 10; D020928:Mitogen-Activated Protein Kinases / Q000037:antagonists & inhibitors / Q000378:metabolism*; D019800:Phenol; D011505:Protein-Tyrosine Kinases / Q000037:antagonists & inhibitors / Q000378:metabolism*; D013778:Tetrazolium Salts / Q000378:metabolism; D014471:Umbilical Veins / Q000166:cytology / Q000378:metabolism
chemical_list: D020533:Angiogenesis Inhibitors; D000873:Anthracenes; D001632:Bibenzyls; C477638:Erianin; D005562:Formazans; D013778:Tetrazolium Salts; C432165:pyrazolanthrone; C079782:MTT formazan; D019800:Phenol; D019344:Lactic Acid; D000255:Adenosine Triphosphate; D048057:Mitogen-Activated Protein Kinase 10; D011505:Protein-Tyrosine Kinases; D020928:Mitogen-Activated Protein Kinases; D005947:Glucose