Effect of Astaxanthin on Anti-Inflammatory and Anti-Oxidative Effects of Astaxanthin Treatment for Atopic Dermatitis-induced MiceEffect of Astaxanthin on Anti-Inflammatory and Anti-Oxidative Effects of Astaxanthin Treatment for Atopic Dermatitis-induced Mice
- Other Titles
- Effect of Astaxanthin on Anti-Inflammatory and Anti-Oxidative Effects of Astaxanthin Treatment for Atopic Dermatitis-induced Mice
- Authors
- 박진우; 송호섭
- Issue Date
- Nov-2021
- Publisher
- 대한침구의학회
- Keywords
- astaxanthin; atopic dermatitis; anti-inflammation anti-oxidative
- Citation
- Journal of Acupuncture Research, v.38, no.4, pp.293 - 299
- Journal Title
- Journal of Acupuncture Research
- Volume
- 38
- Number
- 4
- Start Page
- 293
- End Page
- 299
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/82756
- DOI
- 10.13045/jar.2021.00178
- ISSN
- 2586-288X
- Abstract
- Background: This study sought to determine whether the antioxidant effects of astaxanthin (AST) could have an anti-inflammatory effect to reduce inflammation caused by atopic dermatitis (AD).Methods: Using a mouse model of AD induced by phtalic acid (PA), the levels of inflammation, inflammatory agents, and evidence of antioxidant activity were examined in PA treated mice (n = 3), PA-AST treated mice (n = 3), and a control group of mice (n = 3). This included measurements of ear thickness, levels of mast cells, IgE, inflammatory cytokine, malondialdehyde (MDA), hydrogen peroxide, HO-1, and GPx-1.Results: AST treatment significantly prevented inflammation as measured by ear thickness (p < 0.05), mast cell count (p < 0.001), and IgE concentration in the blood (p < 0.001). Levels of TNF-α (p < 0.001), IL-1β (p < 0.001), IL-6 (p < 0.001), and MDA (p < 0.05) were also significantly lower. In addition, GSH levels increased significantly (p < 0.001), and the level of hydrogen peroxide significantly reduced (p < 0.01). The expression of HO-1, GPx-1 increased.Conclusion: In this small experimental study, AST acted on inflammatory mechanisms that induced AD, through anti-inflammatory and antioxidant mechanisms, and is a candidate of interest in the clinical treatment of AD.
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