Yao Xueming, Wang Qiuyi, Yuan Xuemei, Luo Feng, Ling Yi, Chen Changming, Ma Wukai, Yang Zhu
Department of Rheumatology Immunology, The Second Affiliated Hospital of Guizhou University of Traditional Chinese Medicine, Guiyang, 550001, China.
Guizhou University of Traditional Chinese Medicine, Guiyang, 550025, China.
Inflammopharmacology. 2025 Sep 1. doi: 10.1007/s10787-025-01920-w.
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.
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.
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.
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.
本研究探讨6-姜酚影响间充质干细胞外泌体中微小RNA（miRNA）的机制，以及通过miR-30c-2-3p对滑膜细胞和GES-1中核因子κB（NF-κB）信号通路的调控作用。此外，本研究基于大鼠模型评估6-姜酚对滑膜组织和胃黏膜的潜在保护作用。
采用蛋白质免疫印迹法、透射电子显微镜（TEM）、纳米颗粒跟踪分析（NTA）、实时荧光定量聚合酶链反应（qPCR）、免疫荧光法、双荧光素酶报告基因检测法、酶联免疫吸附测定（ELISA）、CCK-8细胞活力检测法和蛋白质表达分析等实验方法评估6-姜酚的作用。同时，利用动物模型评估6-姜酚对滑膜组织和胃黏膜的影响。
6-姜酚通过上调miR-30c-2-3p、靶向TAB1基因并抑制NF-κB信号通路激活而发挥抗炎作用。在滑膜细胞和GES-1中，6-姜酚均显著降低炎症因子浓度并提高细胞活力。此外，6-姜酚通过miR-30c-2-3p调控NF-κB信号通路中的关键分子，从而减轻炎症反应。基于大鼠模型，6-姜酚对滑膜组织和胃黏膜具有保护作用，而miR-30c-2-3p拮抗剂可能会减弱其治疗效果。
6-姜酚通过上调靶向TAB1的miR-30c-
