Suzuki Ryotaro, Maruyama Kousuke, Sato Soh
Periodontology, Graduate School of Life Dentistry at Niigata, The Nippon Dental University, Chiyoda, Japan.
Department of Periodontology, The Nippon Dental University School of Life Dentistry at Niigata, 1-8 Hamaura-cho, Chou-ku, Niigata, 951-8150, Japan.
Odontology. 2025 Apr;113(2):549-555. doi: 10.1007/s10266-024-00988-0. Epub 2024 Aug 20.
Periodontal disease is an inflammatory disease caused by periodontopathogenic bacteria, the inflammatory response generated against them, and host factors. Furthermore, environmental factors can lead to disease progression. Using lipopolysaccharide (LPS)-stimulated human gingival fibroblast (HGF), this study investigated the bioactivity of HGF after exposure to hesperidin (Hesp) and the anti-inflammatory activity of Hesp against early periodontitis. HGF were cultured in Dulbecco's modified Eagle's medium containing 15% fetal bovine serum. They were exposed to LPS for 6 h, followed by Hesp (1, 10, 30, and 50 µM) exposure for 4 h. Cell proliferation was evaluated using reduction staining with alamerBlue. Inflammatory cytokines [interleukin (IL)-6 and IL-8] and Toll-like receptor 4 (TLR4) levels were assessed using reverse transcription quantitative polymerase chain reaction. Hesp 50 µM + LPS inhibited cell proliferation. The Hesp exposure group inhibited the expression of IL-8 and IL-6. No significant difference in TLR4 expression was observed. Hesp significantly suppressed IL-6 and IL-8 expression by inhibiting downstream signaling without inhibiting TLR4 activation.
牙周病是一种由牙周病原菌、针对这些病原菌产生的炎症反应以及宿主因素引起的炎症性疾病。此外,环境因素可导致疾病进展。本研究使用脂多糖(LPS)刺激的人牙龈成纤维细胞(HGF),研究了橙皮苷(Hesp)作用于HGF后的生物活性以及Hesp对早期牙周炎的抗炎活性。HGF在含有15%胎牛血清的杜氏改良 Eagle培养基中培养。将它们暴露于LPS 6小时,然后暴露于Hesp(1、10、30和50 μM)4小时。使用alamarBlue还原染色评估细胞增殖。使用逆转录定量聚合酶链反应评估炎性细胞因子[白细胞介素(IL)-6和IL-8]和Toll样受体4(TLR4)水平。50 μM Hesp + LPS抑制细胞增殖。Hesp暴露组抑制IL-8和IL-6的表达。未观察到TLR4表达有显著差异。Hesp通过抑制下游信号传导显著抑制IL-6和IL-8的表达,而不抑制TLR4激活。