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Oral administration of Yokukansan inhibits the development of atopic dermatitis-like lesions in isolated NC/Nga mice

Ju JiangabeCorresponding Author Informationemail address, Takuji Yamaguchibd, Naoko Funakushib, Takatoshi Kuharaa, Ping-shen Fanb, Rie Uekic, Hajime Sutoab, Yoshio Kased, Shigaku Ikedaabemail address, Hideoki Ogawaab

Received 11 February 2009; received in revised form 1 July 2009; accepted 3 July 2009. published online 12 July 2010.
Corrected Proof

Refers to erratum:
Erratum to “Oral administration of Yokukansan inhibits the development of atopic dermatitis-like lesions in isolated NC/Nga mice” [J. Dermatol. Sci. 56 (2009) 37–42]
Ju Jiang, Takuji Yamaguchi, Naoko Funakushi, Takatoshi Kuhara, Ping-shen Fan, Rie Ueki, Hajime Suto, Yoshio Kase, Shigaku Ikeda, Hideoki Ogawa
Journal of Dermatological Science
December 2009 (Vol. 56, Issue 3, Page 219)
Full Text | Full-Text PDF (265 KB)

Abstract 

Background

Increasing evidence suggests that stress can trigger and exacerbate atopic dermatitis (AD). Psychotherapy is becoming more important in the treatment of AD patients. Yokukansan (YKS, Yi-Gan San in Chinese), a traditional Japanese medicine, has been widely utilized in the treatment of neurosis, insomnia and anxiety especially in Asian countries. Furthermore, it was reported that YKS inhibited skin lesions in socially isolated mice but not in group-housed mice. Therefore, in the present study it was investigated whether or not YKS was effective in the treatment of AD using socially isolated NC/Nga mice.

Objective

The present study was designed to assess the effect of YKS on the development of AD-like lesions in socially isolated NC/Nga mice to obtain information about its usefulness in the treatment of AD.

Methods

Ten-week-old male NC/Nga mice were socially isolated under conventional conditions. YKS was administered orally to mice at the dose of 0.5% or 1.0% together with diet. The efficacy of YKS was evaluated by assessing skin lesion severity, scratching behaviors, skin hydration, and infiltration of inflammatory cells in the skin. Grooming behaviors evoked by social isolation stress and serum corticosterone levels were also measured.

Results

Oral administration of YKS to socially isolated NC/Nga mice resulted in the inhibition of exacerbation of AD-like skin lesions. It seemed that the inhibition of exacerbation of AD-like skin lesions observed in NC/Nga mice might be due to suppression of the scratching and grooming behaviors, inhibition of the infiltration of mast cells and eosinophils, and retention of humidity in the skin. Serum corticosterone levels were also significantly inhibited in the 1%-YKS-treated mice as compared with those of the control mice. There were no significant differences in the levels of serum total IgE and nerve growth factor (NGF) between the YKS-treated mice and the non-treated control mice.

Conclusion

YKS inhibited the development of AD-like skin lesions in socially isolated NC/Nga mice by suppressing scratching and infiltration of inflammatory cells in the skin. These results indicate that YKS possesses an anti-itching property, and its anti-itching may be partly through attenuation on social isolation stress. It is expected that YKS might provide an effective alternative therapy for AD in human patients.

AbbreviationsYKS, Yokukansan, AD, atopic dermatitis

a Atopy (Allergy) Research Center, Juntendo University School of Medicine, 2-1-1 Hongo, Bunkyo-ku, 113-8421 Tokyo, Japan

b Department of Dermatology, Juntendo University School of Medicine, 2-1-1 Hongo, Bunkyo-ku, 113-8421 Tokyo, Japan

c Dermatology Unit, Juntendo Tokyo Geriatric Medical Center, 3-3-20 Shinsuna, Koto-ku, 136-0075 Tokyo, Japan

d Tsumura Research Laboratories, Tsumura & Co, 3586 Yoshiwara, Ami-machi, Inashiki-gun, 300-1192 Ibaraki, Japan

e Fuzhou Dermatosis Prevention and Control Hospital, 243 Xi Hong Lu, Gu Lou Qu, 350025 FuZhou, China

Corresponding Author InformationCorresponding author at: Atopy (Allergy) Research Center, Juntendo University School of Medicine, 2-1-1 Hongo, Bunkyo-ku, 113-8421 Tokyo, Japan. Tel.: +81 3 5802 1089; fax: +81 3 3813 9443.

PII: S0923-1811(09)00199-6

doi:10.1016/j.jdermsci.2009.07.003