Atopic Dermatitis ( Ad )

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Atopic dermatitis (AD) is a chronic pruritic, inflammatory skin disease caused by various factors. The prevalence of AD has increased 2-3 fold during the past three decades in all over the world (1). A hallmark of AD is dry itchy skin, due at least in part to defects in skin genes that are important for maintaining the barrier function of the skin (2). The pathogenesis of
AD is a complex mechanism. Environmental house dust mite allergen such as
Dermatophagoides farinae (DfE) causes AD in human (3). AD patients are sensitive to DfE and upon exposure, macrophages are known to accumulate in acutely or chronically inflamed skin (4).
Macrophages comprise a heterogeneous population of cells that are widely distributed in different tissues and
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The M2 phenotype is thought to improve tissue repair after inflammation or injury (9).
Galectin-3, a β-galactoside-binding soluble lectin, is highly expressed in activated macrophages, and it has several biological roles including cell proliferation, differentiation, apoptosis, and immune function regulation (10). In addition, galectin-3 also regulates
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alternatively activated M2 macrophage polarization (11). It is critical for the development of allergic inflammatory responses in a mouse model of AD (12).
Flavonoid naringenin is found in most citrus fruits, grape fruit, and tomato skin. The pharmacological effects of naringenin are well known, such as antioxidant, antiinflammatory, anti-mutagenic and anti-carcinogenic activities (13). Its anti-inflammatory property is actively studied in macrophages and ex vivo human whole-blood models (14).
Recent in vitro studies reveal that, the polyphenol naringenin effectively suppressed proinflammatory factors, cytokines and chemokines expressions in inflammation (15).
Moreover, naringenin inhibited the expression and production of thymic stromal lymphopoietin (TSLP) through nuclear factor (NF)
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