Anti-inflammatory effects of Cryptotympana atrata Fabricius slough shed on contact dermatitis induced by dinitrofluorobenzene in mice

Miyoung Kim; Hanna Kim; Jeonghyun Ryu; Suzy Jo; Guemsan Lee; Mi Heon Ryu; Hyungwoo Kim; Su In Cho

Articles

Abstract

Pharmacognosy Magazine,2014,10,38s,s377-s382.

DOI:10.4103/0973-1296.133288

Published:May 2014

Type:Original Article

Authors:

Author(s) affiliations:

Miyoung Kim¹, Hanna Kim¹, Jeonghyun Ryu¹, Suzy Jo¹, Guemsan Lee², Mi Heon Ryu³, Hyungwoo Kim², Su In Cho¹
¹ Division of Pharmacology, School of Korean Medicine, Pusan National University, Gyeongnam, South Korea
² Department of Herbology, College of Korean Medicine, Wonkwang University, Jeonbuk, South Korea
³ Department of Oral Pathology, School of Dentistry, Pusan National University, Gyeongnam, South Korea

Abstract:

Background: The slough shed of Cryptotympana atrata Fabricius is widely used to treat skin diseases in China, Japan, and Korea. Objective: To investigate the anti-inflammatory effects of C. atrata on contact dermatitis. Materials and Methods: We investigated the effects of C. atrata methanol extract (MECA) on ear swelling, histophathological changes and cytokine production in 1-fluoro-2,4-dinitrofluorobenzene (DNFB)-induced contact dermatitis (CD) mice. Results: Topical application of MECA effectively inhibited enlargement of ear swelling (30 and 100 μ/ear, P < 0.05; 300 μg/ear, P < 0.01). MECA treatment also inhibited hyperplasia, spongiosis (100 and 300 μg/ear, P < 0.001), and immune cell infiltration (30 μg/ear, P < 0.05; 100 and 300 μg/ear, P < 0.001) induced by DNFB. In addition, treatment with MECA suppressed the increase in the levels of TNF-α (P < 0.05), IFN-g (3, 100 μg/ear, P < 0.05; 300 μg/ear, P < 0.01), and IL-6 (100 μg/ear, P < 0.05; 300 μg/ear, P < 0.01) production. Conclusion: These data suggest that MECA has the potential for use in the treatment of inflammatory skin diseases, including CD. Moreover, the results presented herein indicate that anti-inflammatory actions of MECA are mediated by decreasing production of TNF-α, IFN-γ, and IL-6 in inflamed tissues.