- P-ISSN 1010-0695
- E-ISSN 2288-3339
Background and Objectives:Atopic dermatitis is a recurrent or chronic eczematous skin disease with severe pruritus,and has increased in Korea. Although the pathogenic mechanisms of atopic dermatitis are yet unknown, recently skin barrier dysfunction and hyperresponsive Th2 cells in the acute phase have been reported as important mechanisms. Cheonggi-san(CGS) is used in oriental clinics for treatingacute skin lesions of eczema or urticaria. There have been no studies on the therapeutic mechanism of CGS for curing atopic dermatitis. We aimed to find out the therapeutic effects of its internaluse on atopic dermatitis-like skin lesions, induced in NC/Nga mice by the mite antigen D. pteronyssinus and disrupting skin barrier. Materials and Methods:The NC/Nga mice were classified into three groups: control group, atopic dermatitis elicitated group(AD), and CGS treated group (CT). Atopic dermatitis-like skin lesions were induced on the back of female NC/Nga mice, 12 weeks of age, by tape stripping, 5% SDS applied to disrupt skin barrier and painting 3 times a week with D. pteronyssinus crude extract solution for 3 weeks. CT was treated with CGS orally after atopic dermatitis was elicitated. We observed changes of skin damage, mast cells, substance P, angiogenesis, skin barrier, Th2 cell differentiation, nuclear factor-κB(NF-κB) p65 activation and COX-2 in NC/Nga mice with atopic dermatitis-like skin lesions. Results:The skin damages as eczema were seenin AD, but mitigated in CT. The degranulated mast cells in dermal papillae increased in AD, but decreased in CT. The substance P positive reacted cells in CT remarkably decreased. The angiogenesis increased in AD, but decreased in CT. The decrease of lipid deposition and ceramide in AD was seen, but anincrease of lipid deposition and ceramide in CT was seen. The distribution of IL-4 positive reacted cells in dermal papillae increased in AD, but decreased in CT. The distribution of NF-κB p65 positive reacted cells & COX-2 positive reacted cells in CT decreased. Conclusion:The results may suggest that the CGS per os decreases the dysfunction of the skin barrier, inhibits Th2 cell differentiation and inhibits NF-κB p65 activation in NC/Nga mice with atopic dermatitis-like skin lesions.
1. 대한피부과학회 교과서 편찬위원회. 개정4판 피부과학. 서울:여문각. 2001:161-166.
2. 박용민. 아토피피부염 병태생리에 대한 최신 지견. 소아알레르기 및 호흡기. 2006;16(3):189-196.
3. Allam JP, Bieber T, Novak N. Recent high- lights in the pathophysiology of atopic eczema. Int Arch Allergy Immunol. 2005;136 :191-7.
4. Qgawa H, Yoshiike T. A speculative view of atopic dermatitis: barrier dysfunction in patho- genesis. J Dermatol Sci. 1993;5:197-204.
5. 김정원. 알레르기 및 면역학적 관점에서의 아토피피부염. 대한피부과학회지. 2003;41(6):687 -689.
6. 차관배, 김윤식, 설인찬. 아토피피부염에 관한 문헌적 고찰. 대전대학교 한의학연구소 논문집. 2005;14(2):113-126.
7. 丁光迪. 諸病源候論校注. 北京:人民衛生出版社. 1994:1411-1412.
8. 陳實功. 外科正宗. 北京:中醫古籍出版社. 1999: 242,261.
9. 吳謙. 醫宗金監. 北京:人民衛生出版社. 1982:443.
10. 박민철, 김진만, 홍철희, 황충연. 아토피피부염의 동서의학적 문헌 고찰. 대한안이비인후피부과학회지. 2002;15(1):226-252.
11. 危亦林. 世醫得效方. 上海:上海科學技術出版社. 1997:962.
12. 최인화, 채병윤. 아토피피부염에 관한 임상적 연구. 대한한의학회지. 1991;12(1):73-83.
13. 김혜정, 채병윤. 淸肌散의 효능에 관한 실험적 연구. 대한한방외관과학회지. 1990;3(1):25-39.
14. 박은정, 김양귀. 淸肌散과 加減淸肌散이 마우스의 항알레르기 및 면역반응에 미치는 영향. 대한한방소아과학회지. 1998;12(1):183-210.
15. 구영희, 홍승욱. 淸肌散이 Th2 세포 분화와 염증에 미치는 영향. 한방안이비인후피부과학회지. 2007;20(3):63-70.
16. 허준. 對譯東醫寶鑑. 서울:법인문화사. 1999:732.
17. 오재원 등. 1995년과 2000년의 학동기와 2003년 학동전기 소아에서의 아토피 피부염의 역학적 변화에 대한 전국적인 연구. 소아알레르기 및 호흡기. 2003;13(4):227-237.
18. 안성구. COMMON SKIN DISEASE. 서울:퍼시픽출판사. 2003:68.
19. 祁坤. 外科大成. 臺北:文光圖書有限公司. 1987: 198,365.
20. 곽동열 편역. 金櫃要略 譯解. 서울:성보사. 2002: 37,457.
21. 王冰 編撰. 新編黃帝內經素問. 서울:대성문화사. 1994:60,105,327.
22. 조용주, 채병윤. 浸淫瘡에 관한 문헌적 고찰. 대한외관과학회지. 1996 ;9(1):114-128.
23. 윤용갑. 동의방제와 처방해설. 서울:의성당. 1998 :583-586.
24. Gopinathan K. M. New insights into skin structure: Scratching the surface. Adv. Drug Delivery Rev. 2002;54:S3-17.
25. Elias P. M., Williams M. L., Maloney M. E., Bonifas J. A., Brown B. E., Grayson S. ans Epstein E. H. Straum corneum lipids in disorders of cornification. J. Clin. Invest. 1984;74:1414-1421.
26. Feinglod K. R. The regulation and role of epidermal lipid synthesis. Adv. Lipid Res. 1998;24:57-82.
27. Paige D. G., Morse-Fisher N., Harper J. I. Quantification of stratum corneum ceramides and lipid envelope ceramide in the hereditary ichthyoses. Br. J. dermatol. 1994;131:23-27.
28. Christophers E. and Mrowietz U. The inflam- matory infiltrate in psoriasis. Clin. Dermatol. 1995;13:131-135.
29. Minehiro O., Takashi Y. and Hideoki O. Detergent-induced epidermal barrier dysfunction and its prevention. J. Dermatol. Sci. 2002;30: 173-179.
30. Donald Y. M and Thomas Bieber. Atopic dermatis. Lancet. 2003;361:151-60.
31. Yoshida S., Ono M., Shono T., Izumi H., Ishibashi T., Suzuki H., Kuwano M. : Involv- ement of IL-8, vascular endothelial growth factor, and basic fibroblast growth factor in TNF-α dependent angiogenesis. Mol. Cell Biol. 1997;17:4015-4023.
32. Misery L. Skin, immunity, and nervous system. Br J Dermatol. 1997;137:843-859.
33. Andrea H., Thomas k., Josef P. and Konrad S. Physiology and pathophysiology of sphingolipid metabolism and signaling. Biochemica et Biophysica Acta. 2000;1485:63-99.
34. Hunnum Y. A. and Bell R. M. Function of sphingolipid breakdown productionin cellular regulation. Science. 1989;243:500-507.
35. Baeuerle P. A. and Baltimore D. NF-κB - Ten years after. Cell. 1996;87:13-20.
36. Baeuerle P. A. IκB-NF-κB structure: at the interface of inflammation control. Cell. 1998; 95:729-731.
37. Z. Morise, S. Komatsu, J. W. Fuseler, D. N. Granger, M. Perry, A.C. Issekutz, and M. B. Grisham. ICAM-1and P-selectin expression in a model of NSAID-induced gastropathy. Am J Physio. 1998;27:G246-252.
38. Tsujii, M., Kawano, S., Tsuji, S., Sawaoka, H., Hori, M., DuBois, R.N. Cyclooxygenase regulates angiogenesis induced by colon cancer cells. Cell 1998;93(5):705-716.
39. 이충은 : JAK-STAT pathway를 경유하는 cyokine과 호르몬의 작용기전. 대한내분비학회. 2000;15 (3):367-387.
40. Friedmann P. S., Tan B. B., Musaba E. Patho- genesis and management of atopic dermatitis. Clin. Exp. Allergy. 1995;25:799-806.