title: [Protective effects of soybean isoflavone on human umbilical vein endothelial cell injury induced by H₂O₂ and lipopolysaccharide].
abstract: OBJECTIVE
  To investigate the protective effects and related mechanisms of soybean isoflavone (SI) on human umbilical vein endothelial cells (HUVECs) injury induced by H₂O₂ and lipopolysaccharide (LPS).
  
  
  METHODS
  H₂O₂ and LPS were used to induce HUVECs injury in vitro. Nine experimental groups were examined: control group, H₂O₂ (2 mmol/L for 4 h), LPS (2 mmol/L for 4 h), H₂O₂+low dose SI (1 mg/ml), H₂O₂+moderate dose SI (2.5 mg/ml), H₂O₂+high dose SI (5 mg/ml), LPS+low dose SI (1 mg/ml), LPS+moderate dose SI (2.5 mg/ml), LPS+high dose SI (5 mg/ml). The survival ratio of HUVECs was detected with MTT assay. The cultured cells were loaded by Fura-2/AM and the change of [Ca²⁺] in HUVECs was measured by fluorospectrophotometry. The contents of malondialdehyde (MDA), superoxide dismutase (SOD), reduced glutathione (GSH-Px) were measured by the commercial kits. The levels of tissue plasminogen activator IL-6 in the supematant were measured by enzyme linked immunosorbent assay (ELISA) kits. Apoptosis rate of the HUVECs was analyzed by flow cytometry.
  
  
  RESULTS
  H₂O₂ and LPS significantly decreased HUVECs viability, increased the contents of MDA, IL-6 and decreased the contents of SOD and GSH-Px, and increased the apoptosis rate [(37.8 ± 1.8)% and (38.9 ± 1.1)%]. Co-treatment with SI could reduce MDA and IL-6 while increase SOD and GSH-Px and reduce apoptosis in a dose-dependent manner.
  
  
  CONCLUSIONS
  The findings demonstrate that soybean isoflavone could attenuate H₂O₂ and LPS induced injury in human umbilical vein endothelial cells through protecting mitochondrial function, improving antioxygenic activity, and suppressing the mobilization of cytosolic calcium.
authors.affiliation: Institute for Biomedical Sciences of Pain, Tangdu Hospital, Fourth Military Medical University, Xi'an 710038, China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Institute for Biomedical Sciences of Pain, Tangdu Hospital, Fourth Military Medical University, Xi'an 710038, China.
authors.forename: Weiping
authors.initials: W
authors.lastname: Bu
authors.affiliation: Institute for Biomedical Sciences of Pain, Tangdu Hospital, Fourth Military Medical University, Xi'an 710038, China.
authors.forename: Hong
authors.initials: H
authors.lastname: Xie
authors.affiliation: Institute for Biomedical Sciences of Pain, Tangdu Hospital, Fourth Military Medical University, Xi'an 710038, China.
authors.forename: Aihua
authors.initials: A
authors.lastname: Qu
authors.affiliation: Institute for Biomedical Sciences of Pain, Tangdu Hospital, Fourth Military Medical University, Xi'an 710038, China. Email:tutuhe@163.com.
authors.forename: Jun
authors.initials: J
authors.lastname: Liu
mesh_terms: D017209:Apoptosis / Q000187:drug effects; D002118:Calcium / Q000378:metabolism; D002478:Cells, Cultured; D061307:Human Umbilical Vein Endothelial Cells / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D006801:Humans; D006861:Hydrogen Peroxide / Q000633:toxicity; D007529:Isoflavones / Q000494:pharmacology*; D015227:Lipid Peroxidation / Q000187:drug effects; D008070:Lipopolysaccharides / Q000633:toxicity; D018384:Oxidative Stress / Q000187:drug effects; D013025:Glycine max / Q000737:chemistry
chemical_list: D007529:Isoflavones; D008070:Lipopolysaccharides; D006861:Hydrogen Peroxide; D002118:Calcium