芦丁通过调节 JAK2/STAT3 信号传导缓解角质形成细胞中与牛皮癣相关的炎症。

IF 2 4区 医学 Q3 DERMATOLOGY
Panhong Wu, Yonghui Liu, Hanxue Zhai, Xiaohan Wu, Aimin Liu
{"title":"芦丁通过调节 JAK2/STAT3 信号传导缓解角质形成细胞中与牛皮癣相关的炎症。","authors":"Panhong Wu, Yonghui Liu, Hanxue Zhai, Xiaohan Wu, Aimin Liu","doi":"10.1111/srt.70011","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Psoriasis is a chronic inflammatory skin disease that can cause systemic inflammation in various organs. Rutin has been suggested to fight psoriasis, but the signaling pathways by which it works need to be explored.</p><p><strong>Materials and methods: </strong>HaCaT cells co-stimulated with interleukin (IL)-17, IL-22, tumor necrosis factor-alpha (TNF-α), IL-1α, and oncostatin M (M5) were used as an in vitro cell model of psoriasis. The proliferation and viability of HaCaT cells were determined by 5-ethynyl-2'-deoxyuridine and cell counting assays. Relative mRNA levels of IL-6, TNF-α, chemokines (CXCL1 and CXCL2), and anti-microbial peptides (S100A7 and S100A8) were detected by reverse transcriptase-quantitative PCR. Release of IL-6 and TNF-α from HaCaT cells was measured by enzyme-linked immunosorbent assay. Keratin1, Keratin5, p-JAK2, and p-STAT3 protein levels were estimated with western blotting. Molecular docking predicted binding sites for Rutin and STAT3.</p><p><strong>Results: </strong>Rutin treatment undercut M5-urged viability increase and proliferation boost in HaCaT cells. Moreover, M5 stimulation mediated upregulation of IL-6, TNF-α, CXCL1, CXCL2, S100A7, and S100A8 was partially reversed after Rutin treatment. In addition, M5 stimulation induced downregulation of Keratin1 and Keratin5 proteins as well as upregulation of p-JAK2 and p-STAT3 proteins were attenuated in response to Rutin treatment, manifesting that Rutin treatment inhibited M5-promoted aberrant differentiation and impaired M5-mediated activation of the JAK2/STAT3 signaling in HaCaT cells. Molecular docking discovered that residues GLN326 and ASP334 in STAT3 might bind to Rutin.</p><p><strong>Conclusion: </strong>Rutin treatment blocked the JAK2/STAT3 signaling, thus attenuating psoriasis-related inflammation and anomalous differentiation in keratinocytes.</p>","PeriodicalId":21746,"journal":{"name":"Skin Research and Technology","volume":null,"pages":null},"PeriodicalIF":2.0000,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11337924/pdf/","citationCount":"0","resultStr":"{\"title\":\"Rutin alleviates psoriasis-related inflammation in keratinocytes by regulating the JAK2/STAT3 signaling.\",\"authors\":\"Panhong Wu, Yonghui Liu, Hanxue Zhai, Xiaohan Wu, Aimin Liu\",\"doi\":\"10.1111/srt.70011\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Psoriasis is a chronic inflammatory skin disease that can cause systemic inflammation in various organs. Rutin has been suggested to fight psoriasis, but the signaling pathways by which it works need to be explored.</p><p><strong>Materials and methods: </strong>HaCaT cells co-stimulated with interleukin (IL)-17, IL-22, tumor necrosis factor-alpha (TNF-α), IL-1α, and oncostatin M (M5) were used as an in vitro cell model of psoriasis. The proliferation and viability of HaCaT cells were determined by 5-ethynyl-2'-deoxyuridine and cell counting assays. Relative mRNA levels of IL-6, TNF-α, chemokines (CXCL1 and CXCL2), and anti-microbial peptides (S100A7 and S100A8) were detected by reverse transcriptase-quantitative PCR. Release of IL-6 and TNF-α from HaCaT cells was measured by enzyme-linked immunosorbent assay. Keratin1, Keratin5, p-JAK2, and p-STAT3 protein levels were estimated with western blotting. Molecular docking predicted binding sites for Rutin and STAT3.</p><p><strong>Results: </strong>Rutin treatment undercut M5-urged viability increase and proliferation boost in HaCaT cells. Moreover, M5 stimulation mediated upregulation of IL-6, TNF-α, CXCL1, CXCL2, S100A7, and S100A8 was partially reversed after Rutin treatment. In addition, M5 stimulation induced downregulation of Keratin1 and Keratin5 proteins as well as upregulation of p-JAK2 and p-STAT3 proteins were attenuated in response to Rutin treatment, manifesting that Rutin treatment inhibited M5-promoted aberrant differentiation and impaired M5-mediated activation of the JAK2/STAT3 signaling in HaCaT cells. Molecular docking discovered that residues GLN326 and ASP334 in STAT3 might bind to Rutin.</p><p><strong>Conclusion: </strong>Rutin treatment blocked the JAK2/STAT3 signaling, thus attenuating psoriasis-related inflammation and anomalous differentiation in keratinocytes.</p>\",\"PeriodicalId\":21746,\"journal\":{\"name\":\"Skin Research and Technology\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":2.0000,\"publicationDate\":\"2024-08-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11337924/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Skin Research and Technology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1111/srt.70011\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"DERMATOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Skin Research and Technology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1111/srt.70011","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"DERMATOLOGY","Score":null,"Total":0}
引用次数: 0

摘要

背景:银屑病是一种慢性炎症性皮肤病,可引起多个器官的系统性炎症。材料与方法:使用白细胞介素(IL)-17、IL-22、肿瘤坏死因子-α(TNF-α)、IL-1α和oncostatin M(M5)共同刺激的 HaCaT 细胞作为银屑病的体外细胞模型。通过 5-乙炔基-2'-脱氧尿苷和细胞计数法测定 HaCaT 细胞的增殖和活力。通过逆转录酶定量 PCR 检测了 IL-6、TNF-α、趋化因子(CXCL1 和 CXCL2)和抗微生物肽(S100A7 和 S100A8)的相对 mRNA 水平。HaCaT 细胞释放的 IL-6 和 TNF-α 通过酶联免疫吸附试验进行检测。角蛋白1、角蛋白5、p-JAK2和p-STAT3的蛋白水平通过蛋白印迹法进行评估。分子对接预测了芦丁和 STAT3 的结合位点:结果:芦丁处理可抑制 M5 引起的 HaCaT 细胞活力增加和增殖促进。此外,M5 刺激介导的 IL-6、TNF-α、CXCL1、CXCL2、S100A7 和 S100A8 的上调在芦丁处理后被部分逆转。此外,M5刺激诱导的Keratin1和Keratin5蛋白下调以及p-JAK2和p-STAT3蛋白的上调在芦丁处理后也有所减弱,这表明芦丁处理抑制了M5促进的异常分化,并损害了M5介导的JAK2/STAT3信号在HaCaT细胞中的激活。分子对接发现,STAT3的残基GLN326和ASP334可能与芦丁结合:结论:芦丁能阻断 JAK2/STAT3 信号传导,从而减轻银屑病相关炎症和角质形成细胞的异常分化。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Rutin alleviates psoriasis-related inflammation in keratinocytes by regulating the JAK2/STAT3 signaling.

Background: Psoriasis is a chronic inflammatory skin disease that can cause systemic inflammation in various organs. Rutin has been suggested to fight psoriasis, but the signaling pathways by which it works need to be explored.

Materials and methods: HaCaT cells co-stimulated with interleukin (IL)-17, IL-22, tumor necrosis factor-alpha (TNF-α), IL-1α, and oncostatin M (M5) were used as an in vitro cell model of psoriasis. The proliferation and viability of HaCaT cells were determined by 5-ethynyl-2'-deoxyuridine and cell counting assays. Relative mRNA levels of IL-6, TNF-α, chemokines (CXCL1 and CXCL2), and anti-microbial peptides (S100A7 and S100A8) were detected by reverse transcriptase-quantitative PCR. Release of IL-6 and TNF-α from HaCaT cells was measured by enzyme-linked immunosorbent assay. Keratin1, Keratin5, p-JAK2, and p-STAT3 protein levels were estimated with western blotting. Molecular docking predicted binding sites for Rutin and STAT3.

Results: Rutin treatment undercut M5-urged viability increase and proliferation boost in HaCaT cells. Moreover, M5 stimulation mediated upregulation of IL-6, TNF-α, CXCL1, CXCL2, S100A7, and S100A8 was partially reversed after Rutin treatment. In addition, M5 stimulation induced downregulation of Keratin1 and Keratin5 proteins as well as upregulation of p-JAK2 and p-STAT3 proteins were attenuated in response to Rutin treatment, manifesting that Rutin treatment inhibited M5-promoted aberrant differentiation and impaired M5-mediated activation of the JAK2/STAT3 signaling in HaCaT cells. Molecular docking discovered that residues GLN326 and ASP334 in STAT3 might bind to Rutin.

Conclusion: Rutin treatment blocked the JAK2/STAT3 signaling, thus attenuating psoriasis-related inflammation and anomalous differentiation in keratinocytes.

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
Skin Research and Technology
Skin Research and Technology 医学-皮肤病学
CiteScore
3.30
自引率
9.10%
发文量
95
审稿时长
6-12 weeks
期刊介绍: Skin Research and Technology is a clinically-oriented journal on biophysical methods and imaging techniques and how they are used in dermatology, cosmetology and plastic surgery for noninvasive quantification of skin structure and functions. Papers are invited on the development and validation of methods and their application in the characterization of diseased, abnormal and normal skin. Topics include blood flow, colorimetry, thermography, evaporimetry, epidermal humidity, desquamation, profilometry, skin mechanics, epiluminiscence microscopy, high-frequency ultrasonography, confocal microscopy, digital imaging, image analysis and computerized evaluation and magnetic resonance. Noninvasive biochemical methods (such as lipids, keratin and tissue water) and the instrumental evaluation of cytological and histological samples are also covered. The journal has a wide scope and aims to link scientists, clinical researchers and technicians through original articles, communications, editorials and commentaries, letters, reviews, announcements and news. Contributions should be clear, experimentally sound and novel.
×
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