Paeonol is a natural phenolic compound in Moutan Cortex with multiple biological functions, such as anti-inflammatory and anti-oxidant activity. Recent evidence has proven that persistent inflammation, oxidative stress, along with nuclear factor E2-related factor 2 (Nrf2) signaling dysfunction in periodontium are the possible causes of alveolar bone resorption, and ultimately lead to periodontitis. The present study was designed to explore the protective effects of paeonol on ligation-induced periodontitis in rats, and investigate the possible mechanism. We found that treatment with paeonol (40, 80 mg/kg, intraperitoneal injection) for 7 days remarkably decreased the expression of receptor activator of nuclear factor kappa-B ligand increased the expression of osteoprotegrin and inhibited the formation of osteoclasts. This function of paeonol might be correlated with its ability to reduce inflammatory factors (IL-1β, IL-6 and TNF-α) and alleviate oxidative stress (SOD, MDA, GSH and ROS) in gingival tissues. Besides, paeonol increased Nrf2 activity. Silence of Nrf2 using specific siRNA diminished the inhibitory effect of paeonol on NF-κB p65 activation and downstream expression, suggesting that Nrf2 was essential for protective effect of paeonol. These results showed that paeonol protected against periodontitis-aggravated osteoclastogenesis and alveolar bone lesion via regulating Nrf2/NF-κB/NFATc1 signaling pathway.

丹皮酚是牡丹皮中的天然酚类化合物，具有多种生物功能，例如抗炎和抗氧化活性。最近的证据证明，牙周炎中持续的炎症，氧化应激以及核因子E2相关因子2（Nrf2）信号功能障碍是牙槽骨吸收的可能原因，并最终导致牙周炎。本研究旨在探讨丹皮酚对结扎诱导的大鼠牙周炎的保护作用，并探讨其可能的机制。我们发现用丹皮酚（40、80 mg / kg，腹膜内注射）治疗7天可显着降低核因子κB配体的受体激活剂的表达，从而增加骨蛋白原蛋白的表达并抑制破骨细胞的形成。丹皮酚的这种功能可能与其减少牙龈组织中的炎性因子（IL-1β，IL-6和TNF-α）和减轻氧化应激（SOD，MDA，GSH和ROS）的能力有关。此外，丹皮酚增加了Nrf2的活性。使用特异性siRNA沉默Nrf2可以降低丹皮酚对NF-κBp65激活和下游表达的抑制作用，这表明Nrf2对于丹皮酚的保护作用至关重要。这些结果表明丹皮酚可通过调节Nrf2 /NF-κB/ NFATc1信号通路来防止牙周炎加重的破骨细胞生成和肺泡骨病变。使用特异性siRNA沉默Nrf2可以降低丹皮酚对NF-κBp65激活和下游表达的抑制作用，这表明Nrf2对于丹皮酚的保护作用至关重要。这些结果表明丹皮酚可通过调节Nrf2 /NF-κB/ NFATc1信号通路来防止牙周炎加重的破骨细胞生成和肺泡骨病变。使用特异性siRNA沉默Nrf2可以降低丹皮酚对NF-κBp65激活和下游表达的抑制作用，这表明Nrf2对于丹皮酚的保护作用至关重要。这些结果表明丹皮酚可通过调节Nrf2 /NF-κB/ NFATc1信号通路来防止牙周炎加重的破骨细胞生成和肺泡骨病变。