동물모델에서 프탈산 무수물에 의해 유도된 아토피 피부염...
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작성자 최고관리자 작성일17-10-17 09:59 조회4,197회 댓글0건관련링크
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Anti-inflammatory effect of Astaxanthin in phthalic anhydride-induced atopic dermatitis animal model
(동물모델에서 프탈산 무수물에 의해 유도된 아토피 피부염에 대한 아스타잔틴의 항명효과)
Experimantal Dermatology에 게재된 논문입니다. 충북대 홍진태 교수님 실험실과 당사가 참여하여 시험한 내용입니다.
Abstract
In this study, we investigated anti-dermatitic effects of Astaxanthin (AST) in phthalic anhydride (PA)-induced atopic dermatitis (AD) animal model as well as in vitro model. AD-like lesion was induced by the topical application of 5% PA to the dorsal skin or ear of Hos:HR-1 mouse. After AD induction, 100 μl of 1 mg/ml and 2 mg/ml of AST (10 μg or 20 μg/cm2) was spread on the dorsum of ear or back skin three times a week for four weeks. We evaluated dermatitis severity, histopathological changes and changes in protein expression by Western blotting for inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and nuclear factor-κB (NF-κB) activity. We also measured tumor necrosis factor- α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), and immunoglobulinE (IgE) concentration in the blood of AD mice by enzyme-linked immunosorbent assay (ELISA). AST treatment attenuated the development of PA-induced AD. Histological analysis showed that AST inhibited hyperkeratosis, mast cells and infiltration of inflammatory cells. AST treatment inhibited expression of iNOS and COX-2, and NF-κB activity as well as release of TNF-α, IL-1β, IL-6, and IgE. In addition, AST (5, 10, and 20μM) potently inhibited lipopolysaccharide (LPS) (1 μg/ml)-induced nitric oxide (NO) production, expression of iNOS and COX-2, and NF-κB DNA binding activities in RAW 264.7 macrophage cells. Our data demonstrated that AST could be a promising agent for AD by inhibition of NF-κB signaling.
(동물모델에서 프탈산 무수물에 의해 유도된 아토피 피부염에 대한 아스타잔틴의 항명효과)
Experimantal Dermatology에 게재된 논문입니다. 충북대 홍진태 교수님 실험실과 당사가 참여하여 시험한 내용입니다.
Abstract
In this study, we investigated anti-dermatitic effects of Astaxanthin (AST) in phthalic anhydride (PA)-induced atopic dermatitis (AD) animal model as well as in vitro model. AD-like lesion was induced by the topical application of 5% PA to the dorsal skin or ear of Hos:HR-1 mouse. After AD induction, 100 μl of 1 mg/ml and 2 mg/ml of AST (10 μg or 20 μg/cm2) was spread on the dorsum of ear or back skin three times a week for four weeks. We evaluated dermatitis severity, histopathological changes and changes in protein expression by Western blotting for inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and nuclear factor-κB (NF-κB) activity. We also measured tumor necrosis factor- α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), and immunoglobulinE (IgE) concentration in the blood of AD mice by enzyme-linked immunosorbent assay (ELISA). AST treatment attenuated the development of PA-induced AD. Histological analysis showed that AST inhibited hyperkeratosis, mast cells and infiltration of inflammatory cells. AST treatment inhibited expression of iNOS and COX-2, and NF-κB activity as well as release of TNF-α, IL-1β, IL-6, and IgE. In addition, AST (5, 10, and 20μM) potently inhibited lipopolysaccharide (LPS) (1 μg/ml)-induced nitric oxide (NO) production, expression of iNOS and COX-2, and NF-κB DNA binding activities in RAW 264.7 macrophage cells. Our data demonstrated that AST could be a promising agent for AD by inhibition of NF-κB signaling.
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