Liu Yaoli, Li Ting, Liao Yilin, Chen Jingqiu, Sheng Yue, Zhao Yaoyu, He Zhenru, Tang Huilin, Wang Yuting, Bian Zhuan, Ji Yaoting
State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education, Hubei Key Laboratory of Stomatology, School & Hospital of Stomatology, Wuhan University, Wuhan, China.
State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education, Hubei Key Laboratory of Stomatology, School & Hospital of Stomatology, Wuhan University, Wuhan, China.
Int Immunopharmacol. 2025 Aug 28;161:115002. doi: 10.1016/j.intimp.2025.115002. Epub 2025 Jun 3.
Periodontitis, one of the most prevalent global disorders, is characterized by oxidative stress-mediated pathogenesis that leads to progressive tissue destruction and bone loss. Given that nuclear factor erythroid 2-related factor 2 (Nrf2) is essential for cellular antioxidant defense, targeting this pathway may represent a promising therapeutic strategy. Sulforaphane (SFN), a natural isothiocyanate with potent antioxidant properties, has been confirmed to be effective against various oxidative stress-related disorders. This study aimed to investigate whether and how SFN attenuates periodontitis progression through Nrf2-mediated antioxidant defense activation. Our study demonstrated that SFN effectively suppressed inflammatory responses induced by Porphyromonas gingivalis Lipopolysaccharides (P. gingivalis LPS) in human gingival fibroblasts (HGFs) in vitro and attenuated periodontitis progression in an experimental rat model. In HGFs, SFN significantly reduced inflammatory mediator production, decreased intracellular and mitochondrial reactive oxygen species (ROS) accumulation, and restored mitochondrial function. Mechanistically, the anti-inflammatory and antioxidant effects of SFN were Nrf2-dependent, as demonstrated by their abolishment in Nrf2-silenced HGFs and enhancement in Nrf2-overexpressing cells. Additionally, SFN alleviated periodontal tissue damage and reduced inflammation in a periodontitis rat model, accompanied by enhanced antioxidant capacity. These results demonstrate that SFN ameliorates periodontitis by activating Nrf2-dependent antioxidant defense, suggesting its therapeutic potential for periodontal treatment.
牙周炎是全球最常见的疾病之一，其特征在于氧化应激介导的发病机制，可导致组织渐进性破坏和骨质流失。鉴于核因子红细胞2相关因子2（Nrf2）对细胞抗氧化防御至关重要，针对该途径可能是一种有前景的治疗策略。萝卜硫素（SFN）是一种具有强大抗氧化特性的天然异硫氰酸盐，已被证实对各种与氧化应激相关的疾病有效。本研究旨在探讨SFN是否以及如何通过Nrf2介导的抗氧化防御激活来减轻牙周炎进展。我们的研究表明，SFN在体外有效抑制牙龈卟啉单胞菌脂多糖（P. gingivalis LPS）诱导的人牙龈成纤维细胞（HGFs）中的炎症反应，并在实验性大鼠模型中减轻牙周炎进展。在HGFs中，SFN显著减少炎症介质产生，降低细胞内和线粒体活性氧（ROS）积累，并恢复线粒体功能。从机制上讲，SFN的抗炎和抗氧化作用依赖于Nrf2，这在Nrf2沉默的HGFs中被消除以及在Nrf2过表达细胞中增强得到证明。此外，SFN减轻了牙周炎大鼠模型中的牙周组织损伤并减少炎症，同时增强了抗氧化能力。这些结果表明，SFN通过激活Nrf2依赖性抗氧化防御来改善牙周炎，表明其在牙周治疗中的治疗潜力。
