title: Protective effects of hyperoside against human umbilical vein endothelial cell damage induced by hydrogen peroxide.
abstract: BACKGROUND
  Hyperoside (Hyp) is a flavonoid compound isolated from Rhododendron ponticum L. leaves that elicits vascular protective effects in vitro. Treatment with Hyp has been found to attenuate endothelial cell damage induced by oxidative stress, but its mechanisms of action remain unclear. This study investigated the action of Hyp in an endothelial injury model induced by hydrogen peroxide (H(2)O(2)), as well as its possible mechanisms.
  
  
  METHODS
  Human umbilical vein endothelial cells (HUVECs) were treated with H(2)O(2) alone or in combination with Hyp. The protective effects of Hyp against H(2)O(2) were evaluated, and the activation of extracellular signal-regulated protein kinase (ERK) in Hyp was assayed in HUVECs.
  
  
  RESULTS
  Loss of cell viability as well as excessive cell apoptosis and death were observed in HUVECs after 18 h of challenge with H(2)O(2) (400μM); however, both cell apoptosis and death were attenuated in the Hyp-pretreated cells. Western blot analysis revealed that Hyp increased the expression of Bcl-2 but decreased that of Bax. In addition, Hyp induced the phosphorylation of ERK1/2 in HUVECs.
  
  
  CONCLUSIONS
  These observations provide preliminary evidence that Hyp protects HUVECs against H(2)O(2) damage, at least partially, by activating the ERK signaling pathway.
authors: Department of Cardiovascular Surgery, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
authors: Zi-lin
authors: ZL
authors: Li
authors: Jin-cheng
authors: JC
authors: Liu
authors: Jing
authors: J
authors: Hu
authors: Xiao-qiang
authors: XQ
authors: Li
authors: Si-wang
authors: SW
authors: Wang
authors: Ding-hua
authors: DH
authors: Yi
authors: Ming-gao
authors: MG
authors: Zhao
mesh_terms: D000975:Antioxidants / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects; D015153:Blotting, Western; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D019610:Cytoprotection; D004305:Dose-Response Relationship, Drug; D004789:Enzyme Activation; D061307:Human Umbilical Vein Endothelial Cells / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D006801:Humans; D006861:Hydrogen Peroxide / Q000633:toxicity*; D019950:Mitogen-Activated Protein Kinase 1 / Q000037:antagonists & inhibitors / Q000378:metabolism; D048052:Mitogen-Activated Protein Kinase 3 / Q000037:antagonists & inhibitors / Q000378:metabolism; D016877:Oxidants / Q000633:toxicity*; D018384:Oxidative Stress / Q000187:drug effects*; D010766:Phosphorylation; D047428:Protein Kinase Inhibitors / Q000494:pharmacology; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D011794:Quercetin / Q000031:analogs & derivatives* / Q000494:pharmacology; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: D000975:Antioxidants; C494826:BAX protein, human; D016877:Oxidants; D047428:Protein Kinase Inhibitors; D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein; C021304:hyperoside; D011794:Quercetin; D006861:Hydrogen Peroxide; C535150:MAPK1 protein, human; D019950:Mitogen-Activated Protein Kinase 1; D048052:Mitogen-Activated Protein Kinase 3