Abstract

The medicinal plant noni (Morinda citrifolia) is widely dispersed throughout Southeast Asia, the Caribbean, and Australia. We previously reported that fermented Noni could alleviate atopic dermatitis (AD) by recovering Th1/Th2 immune balance and enhancing skin barrier function induced by 2,4-dinitrochlorobenzene. Noni has a high deacetylasperulosidic acid (DAA) content, whose concentration further increased in fermented noni as an iridoid constituent. This study aimed to determine the anti-AD effects and mechanisms of DAA on HaCaT, HMC-1, and EOL-1 cells. DAA inhibited the gene expression and secretion of AD-related cytokines and chemokines including interleukin (IL)-1β, IL-4, IL-6, IL-8, IL-25, IL-33, thymic stromal lymphopoietin, tumor necrosis factor-alpha, monocyte chemoattractant protein-1, thymus and activation-regulated chemokine, macrophage-derived chemokine, and regulated upon activation, normal T cell expressed and secreted, in all cells, and inhibited histamine release in HMC-1 cells. DAA controlled mitogen-activated protein kinase phosphorylation levels and the translocation of nuclear factor-kappa light chain enhancer of activated B cells into the nucleus by inhibiting IκBα decomposition in all the cells. Furthermore, DAA increased the expression of proteins involved in skin barrier functions such as filaggrin and involucrin in HaCaT cells. These results confirmed that DAA could relieve AD by controlling immune balance and recovering skin barrier function.

Highlights

  • Atopic dermatitis (AD) is a chronic skin disease that affects many people worldwide [1]

  • Content analysis indicated that the Noni extract powder contained 10.37 ± 0.94 mg/g of deacetylasperulosidic acid (DAA) and 0.98 ± 0.08 mg/g of asperulosidic acid (AA)

  • DAA and AA inhibited the secretion of monocyte chemoattractant protein-1 (MCP-1) and IL-5, and cells treated with 60 nM DAA and AA showed inhibitory effects similar to those treated by 2 nM DEX. These results show that DAA and AA inhibited AD-related cytokines and chemokines in all the cells used in this study

Read more

Summary

Introduction

Atopic dermatitis (AD) is a chronic skin disease that affects many people worldwide [1]. AD generally occurs due to a combination of environmental, genetic, and immunological factors [2,3]. It is accompanied by eczema, erythema, xeroderma, lichenification, and persistent itching [4]. The increase in the level of cytokines released from Th2 cells in AD causes a Th1/Th2 immune imbalance and leads to a lower expression of skin barrier proteins [7]. The restoration of Th1/Th2 immune balance and skin barrier function is the objective of AD treatment. Corticosteroids are the most commonly used drugs for the treatment of AD [14]. Corticosteroids can cause various side effects, such as xeroderma, acne, and depression [15]. The development of anti-AD drugs with fewer side effects is necessary

Objectives
Methods
Results
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call