title: Oral administration of collagen tripeptide improves dryness and pruritus in the acetone-induced dry skin model.
abstract: BACKGROUND
  Dry skin causes pruritus and discomfort in patients with xerosis and atopic dermatitis. General treatment for skin dryness involves the topical application of an emollient. However, more effective, simpler therapies are desired. Collagen tripeptide (CTP) is a highly purified, non-antigenic, low-allergenic collagen fraction that is known to have various biological effects.
  
  
  OBJECTIVE
  To clarify the therapeutic effects of CTP for dry skin using acetone-induced dry skin model mice.
  
  
  METHODS
  ICR mice were treated with acetone followed by oral administration of CTP (80 or 500mg/kg/day) for 3 days. Hyaluronic acid production induced by CTP was assessed using human dermal fibroblasts in vitro and in an acetone-induced dry skin model mice in vivo. Transepidermal water loss (TEWL) and scratching behavior were evaluated. Furthermore, the effects of CTP on intraepidermal nerve fibers and expression of semaphorin 3A (Sema3A) and nerve growth factor (NGF) were examined by immunohistochemistry and quantitative RT-PCR.
  
  
  RESULTS
  CTP enhanced hyaluronic acid production in human dermal fibroblasts in vitro and in murine skin in vivo. Oral administration of CTP in acetone-induced dry skin model mice significantly decreased TEWL and suppressed scratching behavior. Intraepidermal nerve growth was dramatically inhibited in CTP-treated mice. Quantitative PCR analysis and immunohistochemical study revealed that CTP abolished the increased NGF and decreased Sema3A levels induced by acetone treatment.
  
  
  CONCLUSIONS
  Oral administration of CTP improves dry skin and normalizes axon-guidance factors in the epidermis in addition to reducing pruritus. CTP may be used in a new therapeutic strategy against dry skin and pruritus.
authors.affiliation: Department of Environmental Immuno-Dermatology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
authors.forename: Tomoko
authors.initials: T
authors.lastname: Okawa
authors.forename: Yukie
authors.initials: Y
authors.lastname: Yamaguchi
authors.forename: Shinnosuke
authors.initials: S
authors.lastname: Takada
authors.forename: Yasuo
authors.initials: Y
authors.lastname: Sakai
authors.forename: Noriaki
authors.initials: N
authors.lastname: Numata
authors.forename: Fumio
authors.initials: F
authors.lastname: Nakamura
authors.forename: Yoji
authors.initials: Y
authors.lastname: Nagashima
authors.forename: Zenro
authors.initials: Z
authors.lastname: Ikezawa
authors.forename: Michiko
authors.initials: M
authors.lastname: Aihara
mesh_terms: D000096:Acetone / Q000633:toxicity; D000284:Administration, Oral; D000818:Animals; D002478:Cells, Cultured; D024042:Collagen Type I / Q000008:administration & dosage*; D003879:Dermatologic Agents / Q000008:administration & dosage; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D009412:Nerve Fibers / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D020932:Nerve Growth Factor / Q000235:genetics / Q000378:metabolism; D011537:Pruritus / Q000139:chemically induced / Q000188:drug therapy* / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D040121:Semaphorin-3A / Q000235:genetics / Q000378:metabolism; D012867:Skin / Q000187:drug effects / Q000294:innervation / Q000473:pathology; D012871:Skin Diseases / Q000139:chemically induced / Q000188:drug therapy* / Q000235:genetics / Q000378:metabolism; D014867:Water / Q000378:metabolism
chemical_list: D024042:Collagen Type I; D003879:Dermatologic Agents; D012333:RNA, Messenger; C488217:Sema3a protein, mouse; D040121:Semaphorin-3A; C526216:collagen tripeptide Ctp, human; D014867:Water; D000096:Acetone; D020932:Nerve Growth Factor