title: The protective effects of 6-CySeCD with GPx activity against UVB-induced injury in HaCaT cells.
abstract: BACKGROUND
  The generation of harmful reactive oxygen species (ROS) induced by UVB irradiation could induce cell apoptosis and change the cell cycle. 6A,6A'-dicyclohexylamine-6B,6B'-diselenide-bis-β-cyclodextrin (6-CySeCD) is a novel glutathione peroxidase (GPx; EC 1.11.1.9) mimic. The aim of this study was to investigate the anti-oxidative effects of 6-CySeCD in cultured immortalised human keratinocyte cells (HaCaT).
  
  
  METHODS
  HaCaT cells were treated with 30 mJ/cm(2) UVB to establish a damage model. The cultured HaCaT cells were randomly assigned to the control, UVB and treatment groups. The treatment group was incubated with 20 μmol/L of GPx mimics before UVB irradiation. Cell viability was detected by (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, the level of lipid peroxidation was determined by the formation of malondialdehyde (MDA), DNA fragmentation was observed using agarose gel electrophoresis and the levels of intracellular ROS and cell cycle progression were measured by flow cytometry.
  
  
  RESULTS
  The levels of cytotoxicity, intracellular ROS, lipid peroxidation and oxidative DNA damage significantly increased after UVB irradiation in the HaCaT cells. UVB irradiation caused pre-G1 -phase arrest in HaCaT cells and significantly reduced the number of HaCaT cells in the S phase. The GPx mimics 6-CySeCD and 2-phenyl-l,2-benzisoselenazol-3(2H)-one (ebselen) significantly blocked UVB-induced apoptosis and changed the cell cycle of the HaCaT cells. The blocked effect of pretreatment 6-CySeCD in UVB-irradiated HaCaT cells was better than that of pretreatment with ebselen.
  
  
  CONCLUSIONS
  6-CySeCD can relieve the damage induced by UVB irradiation in HaCaT cells.
authors.affiliation: College of Life Science, Key Laboratory for Molecular Enzymology and Engineering of the Ministry of Education, Changchun, China.
authors.forename: Xin
authors.initials: X
authors.lastname: Li
authors.forename: Lin
authors.initials: L
authors.lastname: Zhang
authors.forename: Ya-Wei
authors.initials: YW
authors.lastname: Xu
authors.forename: Cheng
authors.initials: C
authors.lastname: Wang
authors.forename: Yang
authors.initials: Y
authors.lastname: Zhao
authors.forename: Ping
authors.initials: P
authors.lastname: Yu
authors.forename: Shao-Wu
authors.initials: SW
authors.lastname: Lv
authors.forename: Gang-Lin
authors.initials: GL
authors.lastname: Yan
authors.forename: Jun-Qiu
authors.initials: JQ
authors.lastname: Liu
authors.forename: Gui-Min
authors.initials: GM
authors.lastname: Luo
mesh_terms: D017209:Apoptosis / Q000187:drug effects / Q000528:radiation effects; D001393:Azoles / Q000494:pharmacology; D002470:Cell Survival / Q000187:drug effects / Q000528:radiation effects; D002478:Cells, Cultured; D053938:DNA Fragmentation / Q000187:drug effects / Q000528:radiation effects; D059585:G1 Phase Cell Cycle Checkpoints / Q000187:drug effects / Q000528:radiation effects; D006801:Humans; D054833:Isoindoles; D015603:Keratinocytes / Q000187:drug effects* / Q000378:metabolism / Q000528:radiation effects*; D015227:Lipid Peroxidation / Q000187:drug effects; D008315:Malondialdehyde / Q000378:metabolism; D016566:Organoselenium Compounds / Q000494:pharmacology*; D011837:Radiation-Protective Agents / Q000494:pharmacology*; D017382:Reactive Oxygen Species / Q000378:metabolism; D059807:S Phase Cell Cycle Checkpoints / Q000187:drug effects / Q000528:radiation effects; D047392:beta-Cyclodextrins / Q000494:pharmacology*
chemical_list: C586642:6A,6A'-dicyclohexylamine-6B,6B'-diselenide-bis-beta-cyclodextrin; D001393:Azoles; D054833:Isoindoles; D016566:Organoselenium Compounds; D011837:Radiation-Protective Agents; D017382:Reactive Oxygen Species; D047392:beta-Cyclodextrins; C042986:ebselen; D008315:Malondialdehyde