ミノキシジルの発毛作用について  [in Japanese] Hair growth effect of minoxidil  [in Japanese]

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Author(s)

    • 小友 進 OTOMO Susumu
    • 大正製薬(株)特別研究プロジェクト Pharmacological Evaluation Laboratory, Taisho Pharmaceutical Co., Ltd.

Abstract

毛髪の長さと太さは主に毛包サイクルの成長期毛包の期間の長さで決まる.成長期はVEGF,FGF-5S,IGF-1,KGF等の細胞成長因子で維持されている.しかし体内時計によって設定された時が満ちれば,FGF-5,thrombospondin,あるいは何らかの未同定の因子により成長期は終了し,毛母細胞にアポトーシスが誘導され退行期へと移行する.男性型脱毛症は遺伝的背景の下に男性ホルモンによって,より早期に成長期が終了する事によっておこる毛包の矮小化である.ミノキシジルの発毛効果はsulfonylurea receptor(SUR)を作動させ,(2)血管平滑筋ATP感受性Kチャネル開放による毛組織血流改善,(3)毛乳頭細胞からのVEGFなど細胞成長因子の産生促進,(4)ミトコンドリアATP感受性Kチャネル開放による毛母細胞アポトーシス抑制,のいずれかを誘起し,成長期期間を延長して,矮小化毛包を改善することによると推察される.<br>

The length and size of hair are depend on the anagen term in its hair cycle. It has been reported that the some cell growth factors, such as VEGF, FGF-5S, IGF-1 and KGF, induce the proliferation of cells in the matrix, dermal papilla and dermal papillary vascular system and increase the amount of extra cellular matrix in dermal papilla and then maintain follicles in the anagen phase. On the other hand, negative factors, like FGF-5, thrombospondin, or still unknown ones, terminate the anagen phase. If the negative factors become dominant against cell proliferation factors according to fulfilling some time set by the biological clock for hair follicles, TGFβ induced in the matrix tissues evokes apoptosis of matrix cells and shifts the follicles from anagen to catagen. Androgenetic alopecia is caused by miniaturizing of hair follicles located in the frontal or crown part of scalp and are hereditarily more sensitive to androgen. In their hair cycles, the androgen shortens the anagen phase of follicles and shifts them to the catagen phase earlier than usual. The mode of action of hair growth effect of minoxidil is not completely elucidated, but the most plausible explanation proposed here is that minoxidil works as a sulfonylurea receptor (SUR) activator and prolongs the anagen phase of hair follicles in the following manner: minoxidil (1) induces cell growth factors such as VEGF, HGF, IGF-1 and potentiates HGF and IGF-1 actions by the activation of uncoupled SUR on the plasma membrane of dermal papilla cells, (2) inhibits of TGFβ induced apoptosis of hair matrix cells by opening the Kir 6.0 channel pore coupled with SUR on the mitochondrial inner membrane, and (3) dilates hair follicle arteries and increases blood flow in dermal papilla by opening the Kir 6.0 channel pore coupled with SUR on the plasma membrane of vascular smooth muscle cells.<br>

Journal

  • Folia Pharmacologica Japonica

    Folia Pharmacologica Japonica 119(3), 167-174, 2002-03-01

    The Japanese Pharmacological Society

References:  59

Cited by:  4

Codes

  • NII Article ID (NAID)
    10008991664
  • NII NACSIS-CAT ID (NCID)
    AN00198335
  • Text Lang
    JPN
  • Article Type
    Journal Article
  • ISSN
    00155691
  • NDL Article ID
    6087473
  • NDL Source Classification
    ZS51(科学技術--薬学)
  • NDL Call No.
    Z19-247
  • Data Source
    CJP  CJPref  NDL  J-STAGE 
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