title: [Oxidative damage effect of the serum of severe preeclamptic patients on human umbilical vein endothelial cell].
abstract: OBJECTIVE
  To investigate oxidative damage effect of the serum of severe preeclamptic patients on human umbilical vein endothelial cells (HUVEC).
  
  
  METHODS
  (1) HUVEC were randomly divided into 4 groups according to the following: blank group as control, normal group added 20% normal sera of pregnant women, group PE added 20% sera of severe preeclamptic patients, and group PE + Cat added 20% sera of severe preeclamptic patients plus 3×10(3) U/ml catalase. After cultured for 24 hours, the injury morphology and APO2.7 expression of HUVEC were detected by transmission electron microscopy and flow cytometry respectively. (2) Under the real-time scanning by laser scanning confocal microscopy, HUVEC were randomly divided into 4 groups according to the following: control group added 100 µmol/L H2O2 as positive control, normal group, group PE, and group PE + Cat. HUVEC of each group was scanned for 120 seconds to determine levels of reactive oxidative species (ROS), calcium homeostasis, and mitochondria membrane potential.
  
  
  RESULTS
  (1) Obvious injury morphology of HUVEC was observed in group PE, and it was obviously improved by catalase in group PE + Cat. Percentage of HUVEC expressed APO2.7 was (37.8 ± 1.1)% in group PE, which was significantly higher than (13.4 ± 1.1)% in blank group or (13.5 ± 1.5)% in normal group, but significantly lower than (19.2 ± 1.6)% in group PE + Cat (all P < 0.01). (2) The fluorescence intensity curves of intracellular ROS and calcium showed slowly rising in group PE, but no obvious changes in normal group and PE + Cat. The values of ROS and calcium in group PE (12.0 ± 1.3, 4.1 ± 0.7) were higher than those in normal group (1.1 ± 0.4, 0.6 ± 0.4), but lower than those in group PE + Cat (1.5 ± 0.5, 0.9 ± 0.5; all P < 0.01).
  
  
  CONCLUSIONS
  The serum of severe preeclamptic patients caused oxidative damage on HUVEC by increasing intracellular ROS generation, calcium overload, and decreasing mitochondrial membrane potential.
authors.affiliation: Teaching and Research Section of Immunology, Bengbu Medical College, Bengbu 233003, China. qzq7778@yahoo.com.cn
authors.forename: Zhong-qing
authors.initials: ZQ
authors.lastname: Qian
authors.forename: Xin-ping
authors.initials: XP
authors.lastname: Li
authors.forename: Cai-zhi
authors.initials: CZ
authors.lastname: Wang
authors.forename: Xiao-yan
authors.initials: XY
authors.lastname: He
authors.forename: Fang
authors.initials: F
authors.lastname: Fang
mesh_terms: D000328:Adult; D002118:Calcium / Q000378:metabolism; D002374:Catalase / Q000378:metabolism / Q000494:pharmacology*; D002478:Cells, Cultured; D005260:Female; D005434:Flow Cytometry; D061307:Human Umbilical Vein Endothelial Cells / Q000187:drug effects* / Q000378:metabolism; D006801:Humans; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects / Q000502:physiology; D018384:Oxidative Stress; D011225:Pre-Eclampsia / Q000097:blood* / Q000378:metabolism; D011247:Pregnancy; D017382:Reactive Oxygen Species / Q000378:metabolism*; D055815:Young Adult
chemical_list: D017382:Reactive Oxygen Species; D002374:Catalase; D002118:Calcium