Okamoto Risa, Hosokawa Yoshitaka, Hosokawa Ikuko, Ozaki Kazumi, Hosaka Keiichi
Department of Regenerative Dental Medicine, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Tokushima, Japan.
Department of Oral Health Care Promotion, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Tokushima, Japan.
Immunopharmacol Immunotoxicol. 2025 Apr;47(2):176-181. doi: 10.1080/08923973.2024.2445724. Epub 2025 Jan 3.
Periodontal disease is a chronic inflammatory disease caused by periodontopathogenic bacteria, and its progression leads to periodontal tissue destruction and tooth loss. Zerumbone is a bioactive substance found in ginger () and is known to have bioactive effects such as anticancer effects, but there have been no attempts to use it for periodontitis treatment. In addition, there have been no reports examining its effects on periodontal tissue component cells. In this experiment, we aimed to determine whether zerumbone affects the production of inflammatory mediators induced by tumor necrosis factor (TNF)-α in human periodontal ligament cells (HPDLCs), including its effects on signaling pathways.
HPDLCs were stimulated by TNF-α (10 ng/ml) with or without zerumbone (6.25, 12.5, or 25 µM). Cytokine production in supernatant was determined using ELISA. Activation of signal transduction pathways and intracellular protein expression were investigated using the western blot analysis.
Zerumbone significantly suppressed TNF-α-induced production of CC chemokine ligand 2 (CCL2), CCL20, CXC chemokine ligand 10 (CXCL10), and interleukin-6 (IL-6) in HPDLCs. In addition, zerumbone decreased intercellular adhesion molecule-1 (ICAM-1) and cyclooxygenase-2 (COX-2) expression in TNF-α-stimulated HPDLCs. Furthermore, zerumbone suppressed activation of nuclear factor (NF)-κB and signal transducer and activator of transcription 3 (STAT3) pathways in TNF-α-treated HPDLCs. Finally, zerumbone enhanced the production of heme oxygenase-1 (HO-1), an antioxidant enzyme, in HPDLCs.
These results suggest that zerumbone suppressed the production of several inflammatory mediators by inhibiting the NF-κB and STAT3 pathways in HPDLCs.
牙周病是一种由牙周病原菌引起的慢性炎症性疾病，其进展会导致牙周组织破坏和牙齿脱落。姜黄烯是在姜中发现的一种生物活性物质，已知具有抗癌等生物活性作用，但尚未尝试将其用于牙周炎治疗。此外，也没有关于其对牙周组织组成细胞影响的报道。在本实验中，我们旨在确定姜黄烯是否会影响人牙周膜细胞（HPDLCs）中由肿瘤坏死因子（TNF）-α诱导的炎症介质的产生，包括其对信号通路的影响。
用或不用姜黄烯（6.25、12.5或25μM）刺激HPDLCs，并加入TNF-α（10 ng/ml）。使用酶联免疫吸附测定法（ELISA）测定上清液中细胞因子的产生。通过蛋白质印迹分析研究信号转导通路的激活和细胞内蛋白质表达。
姜黄烯显著抑制TNF-α诱导HPDLCs中CC趋化因子配体2（CCL2）、CCL20、CXC趋化因子配体10（CXCL10）和白细胞介素-6（IL-6）的产生。此外，姜黄烯降低了TNF-α刺激的HPDLCs中细胞间黏附分子-1（ICAM-1）和环氧化酶-2（COX-2）的表达。此外，姜黄烯抑制了TNF-α处理的HPDLCs中核因子（NF）-κB和信号转导及转录激活因子3（STAT3）通路的激活。最后，姜黄烯增强了HPDLCs中抗氧化酶血红素加氧酶-1（HO-1）的产生。
这些结果表明，姜黄烯通过抑制HPDLCs中的NF-κB和STAT3通路，抑制了几种炎症介质的产生。
