Anti‐inflammatory effect of astaxanthin in phthalic anhydride‐induced atopic dermatitis animal model. Issue 4 (8th May 2018)

• Record Type: Journal Article
• Authors: Park, Ju Ho; Yeo, In Jun; Han, Ji Hye; Suh, Jeong Won; Lee, Hee Pom; Hong, Jin Tae
• Other Names: Biedermann T. guestEditor.; Kabashima K. guestEditor.
• Is Part Of: Experimental dermatology. Volume 27:Issue 4(2018)
• Page Start: 378
• Page End: 385
• Publication Date: 2018-05-08
• Subjects: astaxanthin -- atopic dermatitis -- cytokine -- IgE -- NF‐κB -- skin inflammation; Dermatology -- Periodicals; 616.5
• DOI: 10.1111/exd.13437
• Languages: English
• ISSNs: 0906-6705

Abstract

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/cm 2 ) 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 immunoglobulin E (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 20 μM) 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 signalling.