戊二醇通过灭活dyrk1a介导的内质网应激,抑制银屑病中角质形成细胞的增殖和炎症反应。

IF 1.3 3区 医学 Q3 CHEMISTRY, APPLIED
Rui Yuan, Qi-Chao Sun, Yue-Peng An, Qing Zhang, Qiong Zhang, Yue Li
{"title":"戊二醇通过灭活dyrk1a介导的内质网应激,抑制银屑病中角质形成细胞的增殖和炎症反应。","authors":"Rui Yuan, Qi-Chao Sun, Yue-Peng An, Qing Zhang, Qiong Zhang, Yue Li","doi":"10.1080/10286020.2024.2446301","DOIUrl":null,"url":null,"abstract":"<p><p>Our work is conducted to reveal the impacts of eriodictyol on psoriasis. CCK-8 and EdU assays measured HaCaT cell proliferation. ELISA detected the activities of inflammatory cytokines and chemokines. Western blot examined the expressions of proliferation-, inflammation- and ERS-associated proteins. Molecular docking predicted the binding affinity of eriodictyol to DYRK1A. RT-qPCR and Western blot analyzed DYRK1A expression. Eriodictyol inhibited the proliferation and inflammatory response in M5-challenged HaCaT cells. Eriodictyol targeted and down-regulated DYRK1A expression. DYRK1A overexpression abolished the impacts of eriodictyol on M5-stimulated HaCaT cells. Conclusively, eriodictyol might suppress ERS mediated by DYRK1A to elicit anti-psoriasis functions.</p>","PeriodicalId":15180,"journal":{"name":"Journal of Asian Natural Products Research","volume":" ","pages":"1-13"},"PeriodicalIF":1.3000,"publicationDate":"2025-02-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Eriodictyol inhibits the proliferation and inflammatory response in keratinocytes in psoriasis through inactivating DYRK1A-mediated endoplasmic reticulum stress.\",\"authors\":\"Rui Yuan, Qi-Chao Sun, Yue-Peng An, Qing Zhang, Qiong Zhang, Yue Li\",\"doi\":\"10.1080/10286020.2024.2446301\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Our work is conducted to reveal the impacts of eriodictyol on psoriasis. CCK-8 and EdU assays measured HaCaT cell proliferation. ELISA detected the activities of inflammatory cytokines and chemokines. Western blot examined the expressions of proliferation-, inflammation- and ERS-associated proteins. Molecular docking predicted the binding affinity of eriodictyol to DYRK1A. RT-qPCR and Western blot analyzed DYRK1A expression. Eriodictyol inhibited the proliferation and inflammatory response in M5-challenged HaCaT cells. Eriodictyol targeted and down-regulated DYRK1A expression. DYRK1A overexpression abolished the impacts of eriodictyol on M5-stimulated HaCaT cells. Conclusively, eriodictyol might suppress ERS mediated by DYRK1A to elicit anti-psoriasis functions.</p>\",\"PeriodicalId\":15180,\"journal\":{\"name\":\"Journal of Asian Natural Products Research\",\"volume\":\" \",\"pages\":\"1-13\"},\"PeriodicalIF\":1.3000,\"publicationDate\":\"2025-02-23\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Asian Natural Products Research\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1080/10286020.2024.2446301\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"CHEMISTRY, APPLIED\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Asian Natural Products Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1080/10286020.2024.2446301","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"CHEMISTRY, APPLIED","Score":null,"Total":0}
引用次数: 0

摘要

我们的工作是为了揭示周期醇对牛皮癣的影响。CCK-8和EdU检测HaCaT细胞增殖。ELISA法检测炎症因子和趋化因子的活性。Western blot检测增殖、炎症和ers相关蛋白的表达。分子对接预测了碘二醇与DYRK1A的结合亲和力。RT-qPCR和Western blot分析DYRK1A的表达。戊二醇抑制m5刺激HaCaT细胞的增殖和炎症反应。周期性醇靶向并下调DYRK1A的表达。DYRK1A过表达消除了周期性醇对m5刺激的HaCaT细胞的影响。总之,周期醇可能抑制DYRK1A介导的ERS,从而引发抗牛皮癣的功能。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Eriodictyol inhibits the proliferation and inflammatory response in keratinocytes in psoriasis through inactivating DYRK1A-mediated endoplasmic reticulum stress.

Our work is conducted to reveal the impacts of eriodictyol on psoriasis. CCK-8 and EdU assays measured HaCaT cell proliferation. ELISA detected the activities of inflammatory cytokines and chemokines. Western blot examined the expressions of proliferation-, inflammation- and ERS-associated proteins. Molecular docking predicted the binding affinity of eriodictyol to DYRK1A. RT-qPCR and Western blot analyzed DYRK1A expression. Eriodictyol inhibited the proliferation and inflammatory response in M5-challenged HaCaT cells. Eriodictyol targeted and down-regulated DYRK1A expression. DYRK1A overexpression abolished the impacts of eriodictyol on M5-stimulated HaCaT cells. Conclusively, eriodictyol might suppress ERS mediated by DYRK1A to elicit anti-psoriasis functions.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
CiteScore
3.20
自引率
5.90%
发文量
47
审稿时长
2.3 months
期刊介绍: The Journal of Asian Natural Products Research (JANPR) publishes chemical and pharmaceutical studies in the English language in the field of natural product research on Asian ethnic medicine. The journal publishes work from scientists in Asian countries, e.g. China, Japan, Korea and India, including contributions from other countries concerning natural products of Asia. The journal is chemistry-orientated. Major fields covered are: isolation and structural elucidation of natural constituents (including those for non-medical uses), synthesis and transformation (including biosynthesis and biotransformation) of natural products, pharmacognosy, and allied topics. Biological evaluation of crude extracts are acceptable only as supporting data for pure isolates with well-characterized structures. All published research articles in this journal have undergone rigorous peer review, based on initial editor screening and anonymized refereeing by at least two expert referees.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信