title: Protective effects of tacalcitol against oxidative damage in human epidermal melanocytes.
abstract: BACKGROUND
  Oxidative damage may lead to the dysfunction of melanocytes (MCs) and is one of the causative mechanisms involved in the pathogenesis of vitiligo.
  
  
  OBJECTIVE
  This study was designed to investigate the protective effects of the vitamin D3 analog tacalcitol on oxidative damage induced by hydrogen peroxide (H2O2) in human epidermal MCs.
  
  
  METHODS
  Human epidermal MCs were cultured and identified by l-DOPA staining and HMB-45 immunohistochemical staining. The model of oxidative damage induced by H2O2was established, and the cells were treated with tacalcitol. The viability of MCs was determined using an MTS assay. Morphological changes in cell dendrites were observed by microscopy, and the rate of change of dendrites was calculated. The reactive oxygen species (ROS) level in MCs was determined using immunofluorescence microscopy. Superoxide dismutase (SOD) activity and malondialdehyde (MDA) levels in MCs were determined using the WST-1 and TBA methods, respectively.
  
  
  RESULTS
  In comparison with the control group, the viability of MCs and SOD activity were significantly decreased in the H2O2group (P < 0.05) and significantly increased in the tacalcitol group (P < 0.05). In comparison with the control group, the rate of change of cell dendrites and levels of ROS and MDA were significantly increased in the H2O2group (P < 0.05) and significantly decreased in the tacalcitol group (P < 0.05).
  
  
  CONCLUSIONS
  Tacalcitol can reduce oxidative damage induced by H2O2in MCs by inhibiting intracellular ROS overproduction, increasing SOD activity, and decreasing the level of MDA, thereby reducing cell apoptosis.
authors.affiliation: Department of Dermatology, Guangzhou Red Cross Hospital, Medical College, Jinan University, Guangzhou, China.
authors.forename: Qi-Lin
authors.initials: QL
authors.lastname: Li
authors.affiliation: Department of Dermatology, Guangzhou Red Cross Hospital, Medical College, Jinan University, Guangzhou, China.
authors.forename: Yan-Hua
authors.initials: YH
authors.lastname: Wu
authors.affiliation: Department of Dermatology, Guangzhou Red Cross Hospital, Medical College, Jinan University, Guangzhou, China.
authors.forename: Mu
authors.initials: M
authors.lastname: Niu
authors.affiliation: Department of Dermatology, Guangzhou Red Cross Hospital, Medical College, Jinan University, Guangzhou, China.
authors.forename: Xiao-Juan
authors.initials: XJ
authors.lastname: Lu
authors.affiliation: Department of Dermatology, Guangzhou Red Cross Hospital, Medical College, Jinan University, Guangzhou, China.
authors.forename: Yong-Hua
authors.initials: YH
authors.lastname: Huang
authors.affiliation: Department of Dermatology, Guangzhou Red Cross Hospital, Medical College, Jinan University, Guangzhou, China.
authors.forename: Dan-Hua
authors.initials: DH
authors.lastname: He
mesh_terms: D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D003712:Dendrites / Q000473:pathology; D004100:Dihydroxycholecalciferols / Q000494:pharmacology*; D000078404:Epidermal Cells; D006801:Humans; D006861:Hydrogen Peroxide / Q000494:pharmacology; D008315:Malondialdehyde / Q000378:metabolism; D008544:Melanocytes / Q000187:drug effects*; D018384:Oxidative Stress / Q000187:drug effects*; D017382:Reactive Oxygen Species / Q000378:metabolism*; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D000893:Anti-Inflammatory Agents; D004100:Dihydroxycholecalciferols; D017382:Reactive Oxygen Species; D008315:Malondialdehyde; C023850:1 alpha,24-dihydroxyvitamin D3; D006861:Hydrogen Peroxide; D013482:Superoxide Dismutase