Dermatology Aspects

Dermatology Aspects

ISSN 2053-5309
Original Research

N-Acetyl-β-endorphin suppresses atopic dermatitis in NC/Nga mice

Keiichi Hiramoto1*, Hiroyuki Yamamoto2 and Kazuaki Iguchi2

*Correspondence: Keiichi Hiramoto

1. Department of Pharmaceutical Science, Suzuka University of Medical Science 3500-3 Minamitamagakicho, Suzuka, Mie 513-8670, Japan.

Author Affiliations

2. Department of Pharmaceutical Science, University of Shizuoka 52-1 Tanida, Shizuoka-shi, Shizuoka 422-8526, Japan.


Background: Atopic dermatitis (AD) is known to be affected by neuropeptides. However, the mechanism underlying this phenomenon is unclear. This study analyzed the mechanism(s) responsible for the influence of β-endorphin (β-End) or N-acetyl-β-endorphin (acetyl-β-End) on AD.

Methods: Specific pathogen-free (SPF) and conventional NC/Nga mice were used for the studies. Conventional (not SPF) mice, spontaneously develop dermal symptoms similar to that of patients with AD. In the present study we treated mice with 5 µg/mouse of β-End or acetyl-β-End for 20 days. In addition, a histone acetyltransferase inhibitor II (HAT inhibitor, 100 mg/kg) was given for 20 days to examine its effects on the acetylation of the β-End.

Results: The symptoms of the conventional group were ameliorated by both β-End and acetyl-β-End treatment, although acetyl-β-End treatment more effectively relieved the symptoms than β-End, and the improvement induced by the β-End treatment disappeared following HAT inhibitor treatment.

Conclusions: These observations suggested that β-End or acetyl-β-End treatment can suppress the symptoms of AD in the mice, and that the effect of the β-End is induced by the acetylation of the β-End by HAT.

Keywords: Atopic dermatitis, β-Endorphin, acetyl-β-Endorphin, histone acetyltransferase inhibitor II

ISSN 2053-5309
Volume 1
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