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通过AKT/mTOR和Jun信号通路对特应性皮炎产生抑制作用。 (推测原文Fermented有误,可能是Inhibited,按照纠正后的词意翻译)

Fermented Against Atopic Dermatitis Through AKT/mTOR and Jun Pathways.

作者信息

Chen Fengfeng, Liu Jing, Yu Xinwei, Jia Honglei, Yang Cheng, Zhao Bingtian

机构信息

Key Laboratory of Synthetic and Biological Colloids, Ministry of Education, School of Chemical and Material Engineering, Jiangnan University, Wuxi 214122, China.

Shanghai Fulai BioHighTech Co., Ltd., Shanghai 201400, China.

出版信息

Pharmaceuticals (Basel). 2024 Dec 27;18(1):20. doi: 10.3390/ph18010020.

DOI:10.3390/ph18010020
PMID:39861084
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11768159/
Abstract

Atopic dermatitis (AD) is a chronic inflammatory skin disorder that has attracted global attention, and alkaloids from have been shown to have anti-inflammatory activity. Fermentation has been used for the structural modification of natural compounds to improve bioavailability and activity, but the AD therapeutic efficacy and mechanism of the fermented (FPN) are still unclear. The potential targets of FPN for AD were preliminarily screened using network pharmacology, and then PCR and WB were used to prove the therapeutic effect of FPN in AD. Network pharmacology indicated that mTOR and Jun were key targets for AD. The experiments in vitro showed that FPN could effectively block AKT/mTOR and AKT/Jun-mediated inflammatory signaling pathways. Moreover, FPN can also alleviate SDS-induced inflammation in zebrafish. It is also found that the anti-inflammatory activity of was enhanced by fermentation, and the oil phase of the fermentation product showed better activity, which may be due to microbial fermentation changing the structure of the original alkaloids. This study elucidated the potential mechanisms of alkaloids derived from fermented against AD; it may also provide a scientific basis for the development of new drugs for AD.

摘要

特应性皮炎(AD)是一种引起全球关注的慢性炎症性皮肤病,并且已证明来自[具体来源未给出]的生物碱具有抗炎活性。发酵已被用于天然化合物的结构修饰以提高生物利用度和活性,但发酵后的[具体物质未给出](FPN)对AD的治疗效果和机制仍不清楚。使用网络药理学初步筛选了FPN对AD的潜在靶点,然后用PCR和WB来证明FPN在AD中的治疗作用。网络药理学表明mTOR和Jun是AD的关键靶点。体外实验表明FPN可以有效阻断AKT/mTOR和AKT/Jun介导的炎症信号通路。此外,FPN还可以减轻SDS诱导的斑马鱼炎症。还发现[具体物质未给出]的抗炎活性通过发酵得到增强,并且发酵产物的油相表现出更好的活性,这可能是由于微生物发酵改变了原始生物碱的结构。本研究阐明了发酵[具体物质未给出]衍生的生物碱抗AD的潜在机制;它也可能为AD新药的开发提供科学依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6636/11768159/ff721e382398/pharmaceuticals-18-00020-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6636/11768159/9cc23560be83/pharmaceuticals-18-00020-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6636/11768159/3a19b5ee8e99/pharmaceuticals-18-00020-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6636/11768159/7804fd5c4633/pharmaceuticals-18-00020-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6636/11768159/99b6779c8973/pharmaceuticals-18-00020-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6636/11768159/a97f59cd011d/pharmaceuticals-18-00020-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6636/11768159/3eb5abd26dd0/pharmaceuticals-18-00020-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6636/11768159/44d50aa850ff/pharmaceuticals-18-00020-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6636/11768159/ff721e382398/pharmaceuticals-18-00020-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6636/11768159/9cc23560be83/pharmaceuticals-18-00020-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6636/11768159/3a19b5ee8e99/pharmaceuticals-18-00020-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6636/11768159/7804fd5c4633/pharmaceuticals-18-00020-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6636/11768159/99b6779c8973/pharmaceuticals-18-00020-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6636/11768159/a97f59cd011d/pharmaceuticals-18-00020-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6636/11768159/3eb5abd26dd0/pharmaceuticals-18-00020-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6636/11768159/44d50aa850ff/pharmaceuticals-18-00020-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6636/11768159/ff721e382398/pharmaceuticals-18-00020-g008.jpg

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