Dione Mactar Ndiaga, Zhang Qi, Shang Sen, Lu Xiaoyun
Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an 710049, China.
Int J Mol Sci. 2024 Nov 28;25(23):12812. doi: 10.3390/ijms252312812.
Inflammation plays an essential role in the phases of rheumatoid arthritis (RA) as the joints secrete a range of molecules that modulate the inflammatory process. While therapies based on physical properties have shown effectiveness in a range of animal experimental models, the understanding of their biological mechanisms remains unclear. The aim of this study was to investigate the immunomodulatory effects of a 0.1 terahertz (THz) wave in rheumatoid arthritis in an attempt to dissect the molecular pathways implicated. The collagen-induced rheumatoid arthritis (CIA) model joint mice were irradiated daily for 30 min over a period of 2 weeks with continuous 0.1 terahertz waves. High-throughput bulk RNA sequencing of the murine blood was performed to analyze and characterize the differences in gene expression changes between the control (Ctrl), CIA (RA), and CIA exposed to THz. Differentially expressed genes, canonical pathway analysis, gene set enrichment, and protein-protein interaction were further run on the selected DEGs. We found that terahertz exposure downregulated gene ontologies representing the "TGF-β signaling pathway", "apoptosis", "activation of T cell receptor signaling pathway", and "non-canonical NF-κB signal transduction". These observations were further confirmed by a decreased level in the expression of transcription factors and , and an increased level of . In addition, the expression of was significantly restored. These results indicate that THz ultimately attenuates the inflammatory response of hemocytes through the T cell and NF-κB pathway, and these changes are reverberated in the blood transcriptome. In this first report of transcriptome sequencing in a model of rheumatoid arthritis exposed to terahertz waves, the downregulated DEGs were associated with anti-inflammatory effects.
炎症在类风湿性关节炎(RA)各阶段发挥着重要作用,因为关节会分泌一系列调节炎症过程的分子。虽然基于物理特性的疗法在一系列动物实验模型中已显示出有效性,但其生物学机制仍不清楚。本研究旨在探讨0.1太赫兹(THz)波对类风湿性关节炎的免疫调节作用,以试图剖析其中涉及的分子途径。采用胶原诱导的类风湿性关节炎(CIA)模型小鼠,在2周时间内每天用连续的0.1太赫兹波照射30分钟。对小鼠血液进行高通量批量RNA测序,以分析和表征对照(Ctrl)、CIA(RA)以及暴露于太赫兹波的CIA之间基因表达变化的差异。对选定的差异表达基因(DEG)进一步进行差异表达基因分析、经典途径分析、基因集富集分析和蛋白质-蛋白质相互作用分析。我们发现,太赫兹波照射下调了代表“TGF-β信号通路”“细胞凋亡”“T细胞受体信号通路激活”和“非经典NF-κB信号转导”的基因本体。转录因子 和 的表达水平降低以及 的表达水平升高进一步证实了这些观察结果。此外, 的表达显著恢复。这些结果表明,太赫兹波最终通过T细胞和NF-κB途径减弱血细胞的炎症反应,并且这些变化在血液转录组中得到体现。在这篇关于太赫兹波照射的类风湿性关节炎模型转录组测序的首次报告中,下调的差异表达基因与抗炎作用相关。