Abstract
Crocin, a major constituent of Gardenia jasminoides, is a natural colorant carotenoid compound that has been reported to have anti-inflammatory effects. This study investigated the therapeutic effects of crocin on mice with atopic dermatitis induced by Dermatophagoides farinae crude extract, which is a common environmental allergen in house dust that causes atopic dermatitis in humans. Crocin application ameliorated Dermatophagoides farinae crude extract-induced atopic dermatitis symptoms by inhibiting the dermatitis severity score, ear thickness, and serum immunoglobulin E levels in NC/Nga mice. The increases in epidermal thickness and dermal inflammatory cells (eosinophil and mast cells) infiltrations observed on the dorsal back skin of atopic dermatitis control mice were inhibited in a dose-dependent manner by topical application of crocin in atopic dermatitis treatment mice. Crocin inhibited the Dermatophagoides farinae crude extract-induced increase of thymus and activation-regulated chemokines, interleukin (IL)-4, and IL-13 on the dorsal skin of mice. Crocin also inhibited Dermatophagoides farinae crude extract-induced activation of nuclear factor-κB (NF-κB) and signal transducer and activator of transcription (STAT) 6. These results show that crocin ameliorates atopic dermatitis symptoms by down regulation of the Th2 cells-mediated immune response via blocking of NF-κB/STAT6 signaling pathways.
Highlights
Atopic dermatitis (AD) is a pruritic, chronic, skin inflammatory disease that includes a prevalentT helper (Th) 2-mediated immune reaction to sustained exposure of allergens [1]
To investigate the effect of crocin treatment on AD-like symptoms, we evaluated the effects of crocin on Dermatophagoides farinae crude extract (DfE)-induced AD model mice (NC/Nga) using clinical features, including dermatitis severity score and ear thickness
Ear thickness increased in the DfE-induced control mice, and the increased ear thickness was significantly reduced by application of 0.3% crocin or TAC (Figure 2c)
Summary
Atopic dermatitis (AD) is a pruritic, chronic, skin inflammatory disease that includes a prevalentT helper (Th) 2-mediated immune reaction to sustained exposure of allergens [1]. Atopic dermatitis (AD) is a pruritic, chronic, skin inflammatory disease that includes a prevalent. Development of AD in infancy and subsequent allergic rhinitis and asthma in later childhood is referred to as the atopic march [3]. This disease is usually characterized by predominant expression of Th2-type cytokines, including interleukin (IL)-4, IL-5, and IL-13, and is associated with elevated circulating immunoglobulin E (IgE) and eosinophilia [4,5]. The development and pathophysiology of AD is complex and multifactorial because it involves dysfunction of the skin barrier, altered immune function, genetic factors, and environmental factors [9].
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