Anti-inflammatory effects of 6-gingerol on arthritis in rats by inhibition of the NF-kB TAB1 signaling pathway.

IF 5.3 2区 医学 Q2 IMMUNOLOGY
Xueming Yao, Qiuyi Wang, Xuemei Yuan, Feng Luo, Yi Ling, Changming Chen, Wukai Ma, Zhu Yang
{"title":"Anti-inflammatory effects of 6-gingerol on arthritis in rats by inhibition of the NF-kB TAB1 signaling pathway.","authors":"Xueming Yao, Qiuyi Wang, Xuemei Yuan, Feng Luo, Yi Ling, Changming Chen, Wukai Ma, Zhu Yang","doi":"10.1007/s10787-025-01920-w","DOIUrl":null,"url":null,"abstract":"<p><strong>Aim: </strong>This study investigated the mechanisms by which 6-gingerol affected miRNAs in mesenchymal stem cell exosomes and the regulation on NF-κB signaling pathways in synovial cells and GES-1 via miR-30c-2-3p. In addition, the study evaluated potential protective effects of 6-gingerol on synovial tissue and gastric mucosa based on a rat model.</p><p><strong>Methods: </strong>The role of 6-gingerol was evaluated using assays including Western Blotting, transmission electron microscopy (TEM), nanoparticle tracking analysis (NTA), qPCR, immunofluorescence, dual luciferase reporter gene assay, ELISA, CCK-8 cell viability assay, and protein expression analysis. Meanwhile, the effects of 6-gingerol on synovial tissue and gastric mucosa were evaluated using an animal model.</p><p><strong>Results: </strong>6-Gingerol exhibited anti-inflammatory effects by upregulating miR-30c-2-3p, targeting the TAB1 gene, and suppressing NF-κB signaling pathway activation. In both synovial cells and GES-1, 6-gingerol significantly reduced the concentration of inflammatory factors and increased cell viability. In addition, 6-gingerol regulated key molecules in the NF-κB signaling pathway through miR-30c-2-3p, thereby reducing inflammatory response. Based on the rat model, 6-gingerol showed protective effects on synovial tissue and gastric mucosa, while miR-30c-2-3p antagomir might attenuate the therapeutic effects.</p><p><strong>Conclusion: </strong>6-Gingerol effectively suppressed the NF-κB signaling pathway activation via upregulating miR-30c-2-3p expression, which targeted TAB1. This led to significant anti-inflammatory and protective effects in synovial cells and GES-1.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":"5599-5619"},"PeriodicalIF":5.3000,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Inflammopharmacology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s10787-025-01920-w","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"IMMUNOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Aim: This study investigated the mechanisms by which 6-gingerol affected miRNAs in mesenchymal stem cell exosomes and the regulation on NF-κB signaling pathways in synovial cells and GES-1 via miR-30c-2-3p. In addition, the study evaluated potential protective effects of 6-gingerol on synovial tissue and gastric mucosa based on a rat model.

Methods: The role of 6-gingerol was evaluated using assays including Western Blotting, transmission electron microscopy (TEM), nanoparticle tracking analysis (NTA), qPCR, immunofluorescence, dual luciferase reporter gene assay, ELISA, CCK-8 cell viability assay, and protein expression analysis. Meanwhile, the effects of 6-gingerol on synovial tissue and gastric mucosa were evaluated using an animal model.

Results: 6-Gingerol exhibited anti-inflammatory effects by upregulating miR-30c-2-3p, targeting the TAB1 gene, and suppressing NF-κB signaling pathway activation. In both synovial cells and GES-1, 6-gingerol significantly reduced the concentration of inflammatory factors and increased cell viability. In addition, 6-gingerol regulated key molecules in the NF-κB signaling pathway through miR-30c-2-3p, thereby reducing inflammatory response. Based on the rat model, 6-gingerol showed protective effects on synovial tissue and gastric mucosa, while miR-30c-2-3p antagomir might attenuate the therapeutic effects.

Conclusion: 6-Gingerol effectively suppressed the NF-κB signaling pathway activation via upregulating miR-30c-2-3p expression, which targeted TAB1. This led to significant anti-inflammatory and protective effects in synovial cells and GES-1.

6-姜辣素通过抑制NF-kB TAB1信号通路对大鼠关节炎的抗炎作用。
目的:研究6-姜辣素影响间充质干细胞外泌体mirna的机制,以及通过miR-30c-2-3p对滑膜细胞和GES-1中NF-κB信号通路的调控作用。此外,本研究还基于大鼠模型评估了6-姜辣素对滑膜组织和胃粘膜的潜在保护作用。方法:采用Western Blotting、透射电镜(TEM)、纳米颗粒跟踪分析(NTA)、qPCR、免疫荧光、双荧光素酶报告基因测定、ELISA、CCK-8细胞活力测定、蛋白表达分析等方法评价6-姜辣素的作用。同时,采用动物模型评价6-姜辣素对滑膜组织和胃粘膜的影响。结果:6-姜辣素通过上调miR-30c-2-3p,靶向TAB1基因,抑制NF-κB信号通路激活,发挥抗炎作用。在滑膜细胞和ges - 1,6 -姜辣素显著降低炎症因子浓度和提高细胞活力。此外,6-姜辣素通过miR-30c-2-3p调节NF-κB信号通路中的关键分子,从而降低炎症反应。在大鼠模型中,6-姜辣素对滑膜组织和胃粘膜有保护作用,而miR-30c-2-3p安塔戈莫可能会减弱其治疗作用。结论:6-姜辣素通过上调miR-30c-2-3p的表达,有效抑制NF-κB信号通路的激活,而miR-30c-2-3p是靶向TAB1的。这导致滑膜细胞和GES-1具有显著的抗炎和保护作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
Inflammopharmacology
Inflammopharmacology IMMUNOLOGYTOXICOLOGY-TOXICOLOGY
CiteScore
8.00
自引率
3.40%
发文量
200
期刊介绍: Inflammopharmacology is the official publication of the Gastrointestinal Section of the International Union of Basic and Clinical Pharmacology (IUPHAR) and the Hungarian Experimental and Clinical Pharmacology Society (HECPS). Inflammopharmacology publishes papers on all aspects of inflammation and its pharmacological control emphasizing comparisons of (a) different inflammatory states, and (b) the actions, therapeutic efficacy and safety of drugs employed in the treatment of inflammatory conditions. The comparative aspects of the types of inflammatory conditions include gastrointestinal disease (e.g. ulcerative colitis, Crohn''s disease), parasitic diseases, toxicological manifestations of the effects of drugs and environmental agents, arthritic conditions, and inflammatory effects of injury or aging on skeletal muscle. The journal has seven main interest areas: -Drug-Disease Interactions - Conditional Pharmacology - i.e. where the condition (disease or stress state) influences the therapeutic response and side (adverse) effects from anti-inflammatory drugs. Mechanisms of drug-disease and drug disease interactions and the role of different stress states -Rheumatology - particular emphasis on methods of measurement of clinical response effects of new agents, adverse effects from anti-rheumatic drugs -Gastroenterology - with particular emphasis on animal and human models, mechanisms of mucosal inflammation and ulceration and effects of novel and established anti-ulcer, anti-inflammatory agents, or antiparasitic agents -Neuro-Inflammation and Pain - model systems, pharmacology of new analgesic agents and mechanisms of neuro-inflammation and pain -Novel drugs, natural products and nutraceuticals - and their effects on inflammatory processes, especially where there are indications of novel modes action compared with conventional drugs e.g. NSAIDs -Muscle-immune interactions during inflammation [...]
×
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:604180095
Book学术官方微信