title: [Impact of sera from children with active Henoch-Schönlein purpura on human umbilical venous endothelial cells (HUVECs) and protective effects of methylprednisolone against HUVECs injury].
abstract: OBJECTIVE
  To observe the changes of human umbilical venous endothelial cells (HUVECs) induced by the sera from children with active Henoch-Sch-nlein purpura (HSP) and the protective effects of methylprednisolone against HUVECs injury.
  
  
  METHODS
  HUVECs were divided into four groups based on the culture conditions: blank control group, normal serum group, HSP serum group, and HSP serum plus methylprednisolone group. The levels of tumor necrosis factor (TNF)-α and interleukin (IL)-8 in the supernatants of each group were detected using ELISA and the nitric oxide (NO) level by nitrate reductase determination. Moreover, the expressions of nuclear factor-kappa B (NF-κB) and Fractalkine in HUVECs were examined by semiquantitative reverse transcription polymerase chain reaction (RT-PCR) and Western blot, respectively.
  
  
  RESULTS
  The levels of IL-8, TNF-α, and NO in the HSP serum group were significantly higher than those in the blank control and normal serum groups (P<0.05). Compared with the HSP serum group, the levels of IL-8, TNF-α, and NO in the HSP serum plus methylprednisolone group decreased significantly (P<0.05). The mRNA expression levels of NF-κB and Fractalkine in the HSP serum group were significantly higher than those in the blank control group (P<0.05). The protein expression levels of NF-κB and Fractalkine in the HSP serum group were significantly higher than those in the blank control and normal control group (P<0.05). Compared with the HSP serum group, the mRNA and protein expression levels of NF-κB and Fractalkine in the HSP serum plus methylprednisolone group decreased significantly (P<0.05).
  
  
  CONCLUSIONS
  The sera from children with active HSP can induce the in vitro cultured HUVECs to become activated and excrete cytokines. Methylprednisolone may inhibit NF-κB expression, reduce the production of inflammatory factors, and thus alleviate vascular inflamation.
authors.affiliation: Department of Pediatrics, First Affiliated Hospital of Anhui Medical University, Hefei 230022, China.
authors.forename: Lin
authors.initials: L
authors.lastname: Wu
authors.forename: Li-Ping
authors.initials: LP
authors.lastname: Yuan
authors.forename: Wen-Jun
authors.initials: WJ
authors.lastname: Fei
authors.forename: Fang
authors.initials: F
authors.lastname: Deng
authors.forename: Qin
authors.initials: Q
authors.lastname: Zhang
authors.forename: Bo
authors.initials: B
authors.lastname: Hu
authors.forename: Ling
authors.initials: L
authors.lastname: Lu
mesh_terms: D002478:Cells, Cultured; D054428:Chemokine CX3CL1 / Q000032:analysis / Q000235:genetics; D002648:Child; D002675:Child, Preschool; D016207:Cytokines / Q000097:blood; D019610:Cytoprotection; D005260:Female; D061307:Human Umbilical Vein Endothelial Cells / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D006801:Humans; D011695:IgA Vasculitis / Q000097:blood*; D008297:Male; D008775:Methylprednisolone / Q000494:pharmacology*; D016328:NF-kappa B / Q000032:analysis / Q000037:antagonists & inhibitors / Q000235:genetics; D009569:Nitric Oxide / Q000502:physiology
chemical_list: D054428:Chemokine CX3CL1; D016207:Cytokines; D016328:NF-kappa B; D009569:Nitric Oxide; D008775:Methylprednisolone