4.7 Article

Dendrobium nobile Lindley Administration Attenuates Atopic Dermatitis-like Lesions by Modulating Immune Cells

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出版社

MDPI
DOI: 10.3390/ijms23084470

关键词

atopic dermatitis; IgE; IL-6; CD4; CD8; HaCaT; cytokine; TARC; GM-CSF; NF-kappa B

资金

  1. National Research Foundation of Korea (NRF) - Korean government (MSIT) [2020R1A2C2005836]
  2. Ministry of Education [2021R1I1A1A01043143]
  3. National Research Foundation of Korea [2020R1A2C2005836] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

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This study confirmed the inhibitory effect of Dendrobium nobile Lindley (DNL) on atopic dermatitis (AD) in mice. The results showed that DNL decreased the levels of IgE, IL-6, and IL-4, as well as scratching behavior and the thickness of the skin. It also inhibited the expression of cytokines and signaling pathways, improving AD symptoms.
Atopic dermatitis (AD) is a chronic inflammatory skin disease that can significantly affect daily life by causing sleep disturbance due to extreme itching. In addition, if the symptoms of AD are severe, it can cause mental disorders such as ADHD and suicidal ideation. Corticosteroid preparations used for general treatment have good effects, but their use is limited due to side effects. Therefore, it is essential to minimize the side effects and study effective treatment methods. Dendrobium nobile Lindley (DNL) has been widely used for various diseases, but to the best of our knowledge, its effect on AD has not yet been proven. In this study, the inhibitory effect of DNL on AD was confirmed in a DNCB-induced Balb/c mouse. In addition, the inhibitory efficacy of inflammatory cytokines in TNF-alpha/IFN-gamma-induced HaCaT cells and PMACI-induced HMC-1 cells was confirmed. The results demonstrated that DNL decreased IgE, IL-6, IL-4, scratching behavior, SCORAD index, infiltration of mast cells and eosinophils and decreased the thickness of the skin. Additionally, DNL inhibited the expression of cytokines and inhibited the MAPK and NF-kappa B signaling pathways. This suggests that DNL inhibits cytokine expression, protein signaling pathway, and immune cells, thereby improving AD symptoms in mice.

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