Kim Tae-Yeon, Kim Eun-Nam, Jeong Gil-Saeng
College of Pharmacy, Chungnam National University, Daejeon 34134, Republic of Korea.
Antioxidants (Basel). 2024 Apr 30;13(5):550. doi: 10.3390/antiox13050550.
Hinokitiol (HKT) is one of the essential oil components found in the heartwood of Cupressaceae plants, and has been reported to have various bioactive effects, including anti-inflammatory effects. However, the improving effect of HKT on periodontitis, which is characterized by periodontal tissue inflammation and alveolar bone loss, has not been clearly revealed. Therefore, we investigated the periodontitis-alleviating effect of HKT and the related molecular mechanisms in human periodontal ligament cells. According to the study results, HKT downregulated SIRT1 and NOX4, which were increased by Lipopolysaccharide (PG-LPS) stimulation and were found to regulate pro-inflammatory mediators and oxidative stress through SIRT1/NOX4 signals. Additionally, by increasing the expression of osteogenic makers such as alkaline phosphatase, osteogenic induction of human periodontal ligament (HPDL) cells, which had been reduced by PG-LPS, was restored. Furthermore, we confirmed that NOX4 expression was regulated through regulation of SIRT1 expression with HKT. The in vitro effect of HKT on improving periodontitis was proven using the periodontal inflammation model, which induces periodontal inflammation using ligature, a representative in vivo model. According to in vivo results, HKT alleviated periodontal inflammation and restored damaged alveolar bone in a concentration-dependent manner in the periodontal inflammation model. Through this experiment, the positive effects of HKT on relieving periodontal tissue inflammation and recovering damaged alveolar bone, which are important treatment strategies for periodontitis, were confirmed. Therefore, these results suggest that HKT has potential in the treatment of periodontitis.
扁柏酚（HKT）是柏科植物心材中发现的精油成分之一，据报道具有多种生物活性，包括抗炎作用。然而，HKT对以牙周组织炎症和牙槽骨丧失为特征的牙周炎的改善作用尚未明确揭示。因此，我们研究了HKT对人牙周膜细胞的牙周炎缓解作用及其相关分子机制。根据研究结果，HKT下调了经脂多糖（PG-LPS）刺激后增加的SIRT1和NOX4，并发现其通过SIRT1/NOX4信号调节促炎介质和氧化应激。此外，通过增加碱性磷酸酶等成骨标志物的表达，恢复了被PG-LPS降低的人牙周膜（HPDL）细胞的成骨诱导作用。此外，我们证实HKT通过调节SIRT1的表达来调节NOX4的表达。使用结扎诱导牙周炎症的牙周炎症模型（一种代表性的体内模型）证明了HKT在体外改善牙周炎的作用。根据体内结果，在牙周炎症模型中，HKT以浓度依赖的方式减轻了牙周炎症并恢复了受损的牙槽骨。通过该实验，证实了HKT在缓解牙周组织炎症和恢复受损牙槽骨方面的积极作用，而这是牙周炎重要的治疗策略。因此，这些结果表明HKT在牙周炎治疗中具有潜力。
