astaxanthine and Dermatitis--Atopic

Pyropia yezoensis, a red alga, is popular and harvested a lot in East Asia and is famous for its medicinal properties attributable to its bioactive compounds including amino acids (porphyra-334 and shinorine, etc.), polysaccharides, phytosterols, and pigments, but its anti-inflammatory effect and mechanism of anti-atopic dermatitis (AD) have not been elucidated. In this study, we investigate the anti-AD effect of P. yezoensis extract (PYE) on mRNA and protein levels of the pro-inflammatory chemokines, thymus, and activation-regulated chemokine (TARC/CCL17) and macrophage-derived chemokine (MDC/CCL22), in human HaCaT keratinocyte cells treated to interferon (IFN)-γ or tumor necrosis factor (TNF)-α (10 ng/mL each). The effect of the PYE on extracellular signal-regulated kinase (ERK) and other mitogen-activated protein kinases (MAPKs) was related to its suppression of TARC and MDC production by blocking NF-κB activation in HaCaT cells. Furthermore, astaxanthin and xanthophyll from P. yezoensis were identified as anti-AD candidate compounds. These results suggest that the PYE may improve AD and contained two carotenoids by regulating pro-inflammatory chemokines.

Topics: Anti-Inflammatory Agents; Chemokine CCL17; Chemokine CCL22; Dermatitis, Atopic; Down-Regulation; Extracellular Signal-Regulated MAP Kinases; HaCaT Cells; Humans; Inflammation Mediators; Interferon-gamma; NF-kappa B; p38 Mitogen-Activated Protein Kinases; Phytotherapy; Plant Extracts; Porphyra; Tumor Necrosis Factor-alpha; Xanthophylls

Previously, we found that astaxanthin (AST) elicited an anti-inflammatory response in an experimental atopic dermatitis (AD) model. However, the use of AST was limited because of low bioavailability and solubility. We hypothesized that liposome formulation of AST could improve this. In this study, we compared the anti-inflammatory and anti-dermatotic effects of liposomal AST (L-AST) and free AST. We evaluated the effect of L-AST on a phthalic anhydride (PA)-induced animal model of AD by analyzing morphological and histopathological changes. We measured the mRNA levels of AD-related cytokines in skin tissue and immunoglobulin E concentrations in the serum. Oxidative stress and transcriptional activities of signal transducer and activator of transcription 3 (STAT3) and nuclear factor (NF)-κB were analyzed

Topics: Animals; Anti-Inflammatory Agents; Cyclooxygenase 2; Cytokines; Dermatitis, Atopic; Disease Models, Animal; Drug Delivery Systems; Liposomes; Male; Mice; Mice, Hairless; NF-kappa B; Nitric Oxide Synthase Type II; Oxidative Stress; Phthalic Anhydrides; Signal Transduction; Skin; STAT3 Transcription Factor; Treatment Outcome; Xanthophylls

Topics: Administration, Cutaneous; Animals; Anti-Inflammatory Agents; Cell Count; Cyclooxygenase 2; Dermatitis, Atopic; Disease Models, Animal; Immunoglobulin E; Interleukin-1beta; Interleukin-6; Lipopolysaccharides; Lymph Nodes; Mast Cells; Mice; NF-kappa B; Nitric Oxide Synthase; Organ Size; Phthalic Anhydrides; RAW 264.7 Cells; Severity of Illness Index; Signal Transduction; Tumor Necrosis Factor-alpha; Xanthophylls

Atopic dermatitis (AD) is a common chronic inflammatory skin disease associated with various factors, including immunological abnormalities and exposure to allergens. Astaxanthin (AST) is a xanthophyll carotenoid that has recently been demonstrated to have anti-inflammatory effects and to regulate the expression of inflammatory cytokines. Thus, we investigated whether AST could improve the dermatitis and pruritus in a murine model of AD using NC/Nga mice. In addition to a behavioral evaluation, the effects of AST on the AD were determined by the clinical skin severity score, serum IgE level, histological analyses of skin, and by reverse transcription-PCR and Western blotting analyses for the expression of inflammation-related factors. AST (100 mg/kg) or vehicle (olive oil) was orally administered once day and three times a week for 26 days. When compared with vehicle-treated group, the administration of AST significantly reduced the clinical skin severity score. In addition, the spontaneous scratching in AD model mice was reduced by AST administration. Moreover, the serum IgE level was markedly decreased by the oral administration of AST compared to that in vehicle-treated mice. The number of eosinophils, total and degranulated mast cells all significantly decreased in the skin of AST-treated mice compared with vehicle-treated mice. The mRNA and protein levels of eotaxin, MIF, IL-4, IL-5 and L-histidine decarboxylase were significantly decreased in the skin of AST-treated mice compared with vehicle-treated mice. These results suggest that AST improves the dermatitis and pruritus in AD via the regulation of the inflammatory effects and the expression of inflammatory cytokines.

Topics: Animals; Anti-Inflammatory Agents; Cytokines; Dermatitis, Atopic; Drug Evaluation, Preclinical; Immunoglobulin E; Male; Mice; Skin; Treatment Outcome; Xanthophylls