Developing an Atopic Dermatitis Model and the Effects of Actinidia Extract on Dermatitis in NC/Nga Mice.
- Author:
Young Hyun JOO
1
;
Chong Hyun WON
;
Ji Yun KIM
;
Kwang Hyun CHO
;
Kyung Up MIN
;
Kyu Han KIM
Author Information
1. Department of Dermatology, Seoul National University College of Medicine, Seoul, Korea. kyuhkim@snu.ac.kr
- Publication Type:In Vitro ; Original Article
- Keywords:
Atopic dermatitis;
Cyclosporine A;
DA-9102;
DNCB;
NC/Nga mice
- MeSH:
Actinidia;
Administration, Oral;
Animals;
Cyclosporine;
Cytokines;
Dermatitis;
Dermatitis, Atopic;
Dinitrochlorobenzene;
Hypersensitivity;
Immunoglobulin E;
Immunoglobulin G;
Interleukin-4;
Mice;
Recurrence;
Skin;
Skin Diseases;
Spleen
- From:Korean Journal of Dermatology
2009;47(10):1105-1112
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Atopic dermatitis is a chronic itchy, inflammatory skin disease that usually relapses. Although the etiology of atopic dermatitis remains unclear, it has been shown that both Th1 and Th2 cytokines play pathogenic roles in the generation of atopic dermatitis. DA-9102 is a fraction from the Actinidia species and DA-9102 displays immune modulating activity for allergy related disease. OBJECTIVE: We have developed the atopic dermatitis model of NC/Nga mice using DNCB and we examined whether DA-9102 suppresses the development of atopic dermatitis-like skin lesions on NC/Nga mice. METHODS: NC/Nga mice were challenged with DNCB during 5 weeks to develop atopic dermatitis-like skin lesions. Daily DA-9102 or cyclosporine A or HPMC (control) were then given orally. The efficacy of DA-9102 in NC/Nga mice was judged by measurement of the skin lesion severity (a modified SCORAD score), the serum IgE and IgG2a levels and the cytokine levels (IFN-gamma and IL-4) from spleen cells cultured with ConA. RESULTS: Atopic dermatitis-like lesions were developed on the NC/Nga mice by using topical DNCB. Oral administration of 100 mg/kg DA-9102 significantly suppressed the development of dermatitis, as was analyzed by a modified SCORAD score (p<0.01). The serum IgE level increased gradually with age, but treatment with DA-9102 suppressed the increment of the serum IgE level (p<0.01). The mean values of IFN-gamma in the NC/Nga mice of the DA-9102 group were lower than those of the control mice group (p<0.05). The mean values of IL-4 were undetectable in all the experimental groups. The serum IgG2a level were not significantly different among all the experimental groups. CONCLUSION: We successfully developed an atopic dermatitis model in NC/Nga mice. Based on our in in vitro data, we suggest that DA-9102 can be useful for the treatment of atopic dermatitis.
