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출처 : http://www.plosone.org/home.action
자료위치1: http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0016377
자료위치2: http://dl.dropbox.com/u/13640483/journal.pone.0016377.pdf

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Abstract
Corticotropin-releasing factor (CRF) signaling pathways are involved in the stress response, and there is growing evidence
supporting hair growth inhibition of murine hair follicle in vivo upon stress exposure. We investigated whether the blockade
of CRF receptors influences the development of hair loss in CRF over-expressing (OE)-mice that display phenotypes of
Cushing’s syndrome and chronic stress, including alopecia. The non-selective CRF receptors antagonist, astressin-B (5 mg/
mouse) injected peripherally once a day for 5 days in 4–9 months old CRF-OE alopecic mice induced pigmentation and hair
re-growth that was largely retained for over 4 months. In young CRF-OE mice, astressin-B prevented the development of
alopecia that occurred in saline-treated mice. Histological examination indicated that alopecic CRF-OE mice had hair follicle
atrophy and that astressin-B revived the hair follicle from the telogen to anagen phase. However, astressin-B did not show
any effect on the elevated plasma corticosterone levels and the increased weights of adrenal glands and visceral fat in CRFOE
mice. The selective CRF2 receptor antagonist, astressin2-B had moderate effect on pigmentation, but not on hair regrowth.
The commercial drug for alopecia, minoxidil only showed partial effect on hair re-growth. These data support the
existence of a key molecular switching mechanism triggered by blocking peripheral CRF receptors with an antagonist to
reset hair growth in a mouse model of alopecia associated with chronic stress.

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