title: Inhibitory effects of UV-based therapy on dry skin-inducible nerve growth in acetone-treated mice.
abstract: BACKGROUND
  UV-based therapy has anti-pruritic effects in inflammatory skin diseases, such as atopic dermatitis and psoriasis. These anti-pruritic effects may be partly due to inhibition of intraepidermal nerve growth, but they have not been fully characterized.
  
  
  OBJECTIVE
  This study was performed to characterize the anti-nerve growth effects of UV-based therapies in acetone-treated mice as an acute dry skin model.
  
  
  METHODS
  Nerve fibers penetrate into the epidermis 24h after acetone treatment in mice, and nerve growth peaks 48h after acetone treatment. To investigate the effects of UV-based therapies on the epidermal nerve fibers, including combination treatment with corticosteroid ointment, the mice were treated with psoralen ultraviolet A (PUVA), PUVA and betamethasone valerate ointment (PUVA+BV), narrowband ultraviolet B (NB-UVB), or an excimer lamp. Each therapy was provided 24h after acetone treatment, and skin samples were taken 48h later. Nerve fiber densities and expression levels of nerve growth factor (NGF) and semaphorin 3A (Sema3A) in the epidermis were examined by immunohistochemistry.
  
  
  RESULTS
  Penetration of nerve fibers into the epidermis was observed in the acetone-treated mice, concomitant with increased NGF and decreased Sema3A levels in the epidermis. The acetone-induced intraepidermal nerve growth was significantly decreased by PUVA, PUVA+BV, NB-UVB, and excimer lamp treatments compared with controls. In addition, PUVA+BV and NB-UVB normalized the abnormal expression of NGF and Sema3A in the epidermis, but no such normalization was observed with excimer lamp treatment.
  
  
  CONCLUSIONS
  UV-based therapies, especially NB-UVB and excimer lamp treatments, may be effective therapeutic methods for pruritus involving epidermal hyperinnervation.
authors: Institute for Environmental and Gender Specific Medicine, Juntendo University Graduate School of Medicine, 2-1-1 Tomioka, Urayasu, Chiba 279-0021, Japan.
authors: Atsuko
authors: A
authors: Kamo
authors: Mitsutoshi
authors: M
authors: Tominaga
authors: Suhandy
authors: S
authors: Tengara
authors: Hideoki
authors: H
authors: Ogawa
authors: Kenji
authors: K
authors: Takamori
mesh_terms: D000096:Acetone / Q000494:pharmacology*; D000305:Adrenal Cortex Hormones / Q000627:therapeutic use; D000818:Animals; D001624:Betamethasone Valerate / Q000494:pharmacology; D003876:Dermatitis, Atopic / Q000188:drug therapy*; D004817:Epidermis / Q000378:metabolism; D005363:Ficusin / Q000494:pharmacology; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D020932:Nerve Growth Factor / Q000378:metabolism; D009474:Neurons / Q000378:metabolism* / Q000473:pathology; D040121:Semaphorin-3A / Q000378:metabolism; D012867:Skin / Q000473:pathology*; D014466:Ultraviolet Rays
chemical_list: D000305:Adrenal Cortex Hormones; D040121:Semaphorin-3A; D000096:Acetone; D020932:Nerve Growth Factor; D001624:Betamethasone Valerate; D005363:Ficusin