Huang Liang-Gie, Yu Cheng-Chia, Fang Jia-You, Ng Min Yee, Liao Yi-Wen, Chang Yu-Chao
School of Dentistry, Chung Shan Medical University, Taichung, Taiwan.
Department of Stomatology, Taichung Veterans General Hospital, Taichung, Taiwan.
J Dent Sci. 2025 Jul;20(3):1853-1860. doi: 10.1016/j.jds.2025.04.022. Epub 2025 May 21.
BACKGROUND/PURPOSE: Individuals with diabetes mellitus (DM) are more susceptible to periodontitis, largely due to the accumulation of advanced glycation end-products (AGEs), which drive oxidative stress and inflammaging. Inflammaging is a state of chronic low-grade inflammation and accelerated cellular aging that contributes to periodontal degradation, mediated by AGEs-induced cellular senescence and senescence-associated secretory phenotype (SASP). 2-O-methylmagnolol (2-MG), a bioactive compound with antioxidant and anti-inflammatory properties, remains underexplored in DM-associated periodontal degeneration. This study investigated the effects of 2-MG on AGE-induced oxidative stress and inflammaging in human gingival epithelial cells (HGEs) and human gingival fibroblasts (HGFs).
The study assessed the effects of 2-MG on AGE-stimulated HGEs and HGFs by evaluating cell proliferation, wound healing capacity, reactive oxygen species (ROS) accumulation, cellular senescence markers, and the secretion of SASP factors, including interleukin (IL)-6 and IL-8. Additionally, Western blot analysis was performed to examine the protein expression of a senescence marker p16.
Treatment with 2-MG at concentrations up to 10 μM did not significantly affect HGEs and HGFs cell proliferation ( > 0.05). However, 2-MG effectively improved AGEs-induced wound healing impairment and significantly attenuated ROS production in a dose-dependent manner ( < 0.05). Furthermore, 2-MG reduced cellular senescence and suppressed the secretion of IL-6 and IL-8 ( < 0.05). Western blot analysis demonstrated that 2-MG inhibited AGEs-induced p16 expression ( < 0.05).
The findings indicate that 2-MG mitigates AGEs-induced oxidative stress and inflammaging in HGEs and HGFs. These results suggest that 2-MG may have therapeutic potential in preventing or attenuating DM-associated periodontal degeneration.
背景/目的：糖尿病（DM）患者更容易患牙周炎，这主要是由于晚期糖基化终产物（AGEs）的积累，AGEs会引发氧化应激和炎症衰老。炎症衰老是一种慢性低度炎症和细胞加速衰老的状态，由AGEs诱导的细胞衰老和衰老相关分泌表型（SASP）介导，从而导致牙周组织退化。2-O-甲基厚朴酚（2-MG）是一种具有抗氧化和抗炎特性的生物活性化合物，在糖尿病相关的牙周组织退化方面仍未得到充分研究。本研究调查了2-MG对AGEs诱导的人牙龈上皮细胞（HGEs）和人牙龈成纤维细胞（HGFs）氧化应激和炎症衰老的影响。
本研究通过评估细胞增殖、伤口愈合能力、活性氧（ROS）积累、细胞衰老标志物以及SASP因子（包括白细胞介素（IL）-6和IL-8）的分泌，来评估2-MG对AGEs刺激的HGEs和HGFs的影响。此外，进行蛋白质印迹分析以检测衰老标志物p16的蛋白表达。
浓度高达10 μM的2-MG处理对HGEs和HGFs的细胞增殖没有显著影响（>0.05）。然而，2-MG有效地改善了AGEs诱导的伤口愈合损伤，并以剂量依赖的方式显著减弱了ROS的产生（<0.05）。此外，2-MG减少了细胞衰老，并抑制了IL-6和IL-8的分泌（<0.05）。蛋白质印迹分析表明，2-MG抑制了AGEs诱导的p-16表达（<0.05）。
研究结果表明，2-MG减轻了AGEs诱导的HGEs和HGFs氧化应激和炎症衰老。这些结果表明，2-MG在预防或减轻糖尿病相关的牙周组织退化方面可能具有治疗潜力。
