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反式-丁香烯抑制人角质形成细胞 AHR 信号通路并激活 NRF2 抗氧化通路。

Perillaldehyde Inhibits AHR Signaling and Activates NRF2 Antioxidant Pathway in Human Keratinocytes.

机构信息

Department of Dermatology, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashiku, Fukuoka 812-8582, Japan.

Research and Clinical Center for Yusho and Dioxin, Kyushu University Hospital, 3-1-1 Maidashi, Higashiku, Fukuoka 812-8582, Japan.

出版信息

Oxid Med Cell Longev. 2018 Feb 14;2018:9524657. doi: 10.1155/2018/9524657. eCollection 2018.

DOI:10.1155/2018/9524657
PMID:29643980
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5832143/
Abstract

The skin covers the outer surface of the body, so the epidermal keratinocytes within it are susceptible to reactive oxygen species (ROS) generated by environmental pollutants such as benzo(a)pyrene (BaP), a potent activator of aryl hydrocarbon receptor (AHR). Antioxidant activity is generally mediated by the nuclear factor-erythroid 2-related factor-2 (NRF2) and heme oxygenase-1 (HO1) axis in human keratinocytes. Perillaldehyde is the main component of , which is a medicinal antioxidant herb traditionally consumed in East Asia. However, the effect of perillaldehyde on the AHR/ROS and/or NRF2/HO1 pathways remains unknown. In human keratinocytes, we found that perillaldehyde (1) inhibited BaP-induced AHR activation and ROS production, (2) inhibited BaP/AHR-mediated release of the CCL2 chemokine, and (3) activated the NRF2/HO1 antioxidant pathway. Perillaldehyde is thus potentially useful for managing inflammatory skin diseases or disorders related to oxidative stress.

摘要

皮肤覆盖在身体的外表面,因此其中的表皮角质形成细胞容易受到环境污染物(如苯并(a)芘(BaP))产生的活性氧(ROS)的影响,BaP 是芳烃受体(AHR)的有效激活剂。抗氧化活性通常由人类角质形成细胞中的核因子-红细胞 2 相关因子 2(NRF2)和血红素加氧酶-1(HO1)轴介导。紫苏醛是紫苏醛的主要成分,紫苏醛是一种传统上在东亚食用的药用抗氧化草药。然而,紫苏醛对 AHR/ROS 和/或 NRF2/HO1 途径的影响尚不清楚。在人类角质形成细胞中,我们发现紫苏醛(1)抑制 BaP 诱导的 AHR 激活和 ROS 产生,(2)抑制 BaP/AHR 介导的趋化因子 CCL2 的释放,以及(3)激活 NRF2/HO1 抗氧化途径。因此,紫苏醛可能有助于治疗与氧化应激相关的炎症性皮肤病或疾病。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed60/5832143/01ecb1950c06/OMCL2018-9524657.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed60/5832143/1292514529b7/OMCL2018-9524657.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed60/5832143/2f5a8bb329d5/OMCL2018-9524657.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed60/5832143/78740e99de6c/OMCL2018-9524657.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed60/5832143/80b7f84c36c8/OMCL2018-9524657.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed60/5832143/01ecb1950c06/OMCL2018-9524657.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed60/5832143/1292514529b7/OMCL2018-9524657.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed60/5832143/2f5a8bb329d5/OMCL2018-9524657.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed60/5832143/78740e99de6c/OMCL2018-9524657.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed60/5832143/80b7f84c36c8/OMCL2018-9524657.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed60/5832143/01ecb1950c06/OMCL2018-9524657.005.jpg

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