title: Chronic restraint stress inhibits hair growth via substance P mediated by reactive oxygen species in mice.
abstract: BACKGROUND
  Solid evidence has demonstrated that psychoemotional stress induced alteration of hair cycle through neuropeptide substance P (SP) mediated immune response, the role of reactive oxygen species (ROS) in brain-skin-axis regulation system remains unknown.
  
  
  OBJECTIVE
  The present study aims to investigate possible mechanisms of ROS in regulation of SP-mast cell signal pathway in chronic restraint stress (CRS, a model of chronic psychoemotional stress) which induced abnormal of hair cycle.
  
  
  RESULTS
  Our results have demonstrated that CRS actually altered hair cycle by inhibiting hair follicle growth in vivo, prolonging the telogen stage and delaying subsequent anagen and catagen stage. Up-regulation of SP protein expression in cutaneous peripheral nerve fibers and activation of mast cell were observed accompanied with increase of lipid peroxidation levels and reduction of the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in CRS mice skin. In addition, SP receptor antagonist (RP67580) reduced mast cell activations and lipid peroxidation levels as well as increased GSH-Px activity and normalized hair cycle. Furthermore, antioxidant Tempol (a free radical scavenger) also restored hair cycle, reduced SP protein expression and mast cell activation.
  
  
  CONCLUSIONS
  Our study provides the first solid evidence for how ROS play a role in regulation of psychoemotional stress induced SP-Mast cell pathway which may provide a convincing rationale for antioxidant application in clinical treatment with psychological stress induced hair loss.
authors: Department of Clinical Psychology, Medical College of Soochow University, Suzhou, PR China.
authors: Nan
authors: N
authors: Liu
authors: Lin-Hui
authors: LH
authors: Wang
authors: Ling-Ling
authors: LL
authors: Guo
authors: Guo-Qing
authors: GQ
authors: Wang
authors: Xi-Ping
authors: XP
authors: Zhou
authors: Yan
authors: Y
authors: Jiang
authors: Jing
authors: J
authors: Shang
authors: Koji
authors: K
authors: Murao
authors: Jing-Wei
authors: JW
authors: Chen
authors: Wen-Qing
authors: WQ
authors: Fu
authors: Guo-Xing
authors: GX
authors: Zhang
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D002908:Chronic Disease; D003345:Corticosterone / Q000097:blood; D020405:Dermis / Q000187:drug effects / Q000201:enzymology / Q000473:pathology; D005979:Glutathione Peroxidase / Q000378:metabolism; D006197:Hair / Q000187:drug effects / Q000254:growth & development* / Q000378:metabolism; D018859:Hair Follicle / Q000187:drug effects / Q000254:growth & development / Q000473:pathology; D008297:Male; D008407:Mast Cells / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D064729:Neurokinin-1 Receptor Antagonists; D018384:Oxidative Stress / Q000187:drug effects; D017382:Reactive Oxygen Species / Q000378:metabolism*; D018040:Receptors, Neurokinin-1 / Q000378:metabolism; D012149:Restraint, Physical; D013315:Stress, Psychological / Q000097:blood / Q000378:metabolism* / Q000473:pathology*; D013373:Substance P / Q000378:metabolism*; D013482:Superoxide Dismutase / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D015430:Weight Gain / Q000187:drug effects
chemical_list: D000975:Antioxidants; D064729:Neurokinin-1 Receptor Antagonists; D017382:Reactive Oxygen Species; D018040:Receptors, Neurokinin-1; D017392:Thiobarbituric Acid Reactive Substances; D013373:Substance P; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D003345:Corticosterone
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