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鞣花酸通过 MAPK 和 STAT 通路对角质形成细胞的抗炎作用。

Anti-Inflammatory Effects of Ellagic Acid on Keratinocytes via MAPK and STAT Pathways.

机构信息

Department of Pharmacology, College of Korean Medicine, Sangji University, Wonju-si 26339, Gangwon-do, Korea.

Department of Korean Meidicne Ophthalmology & Otolaryngology & Dermatology, College of Korean Medicine, Sangji University, Wonju-si 26339, Gangwon-do, Korea.

出版信息

Int J Mol Sci. 2021 Jan 28;22(3):1277. doi: 10.3390/ijms22031277.

DOI:10.3390/ijms22031277
PMID:33525403
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7865693/
Abstract

Atopic dermatitis (AD) is a chronic inflammatory skin disease that is characterized by an impaired skin barrier and intense itchiness, which decreases the individual's quality of life. No fully effective therapeutic agents have prevailed for AD due to an insufficient grasp of the complex etiology. Ellagic acid (EA), a natural compound, has anti-inflammatory properties in chronic diseases. The effects of EA on AD have not yet been explored. The present study investigated the effects of EA on TNF-α/IFN-γ-stimulated HaCaT keratinocytes and house dust mite-induced AD-like skin lesions in NC/Nga mice. Treatment with EA suppressed inflammatory responses in keratinocytes by regulating critical inflammatory signaling pathways, such as mitogen-activated protein kinases and signal transducers and activators of transcription. In vivo studies using a DfE-induced AD mouse model showed the effects of EA administration through ameliorated skin lesions via decremented histological inflammatory reactions. These results suggest that EA could be a potential therapeutic alternative for the treatment of AD by inhibiting inflammatory signaling pathways.

摘要

特应性皮炎（AD）是一种慢性炎症性皮肤病，其特征为皮肤屏障受损和剧烈瘙痒，从而降低个体的生活质量。由于对复杂病因的认识不足，目前尚无完全有效的治疗药物用于 AD。鞣花酸（EA）是一种天然化合物，在慢性疾病中有抗炎作用。EA 对 AD 的影响尚未得到探索。本研究探讨了 EA 对 TNF-α/IFN-γ 刺激的 HaCaT 角质形成细胞和屋尘螨诱导的 NC/Nga 小鼠 AD 样皮肤损伤的影响。EA 通过调节丝裂原活化蛋白激酶和信号转导和转录激活因子等关键炎症信号通路，抑制角质形成细胞中的炎症反应。使用 DfE 诱导的 AD 小鼠模型进行的体内研究表明，通过减轻组织学炎症反应，EA 可通过改善皮肤损伤来发挥作用。这些结果表明，EA 通过抑制炎症信号通路，可能成为治疗 AD 的一种有潜力的治疗选择。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1327/7865693/bc42264d908e/ijms-22-01277-g005.jpg
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