Liu Caiye, Chen Yi, Wang Ying, Wang Danyang, Sun Jinyan, Sun Jiao, Ji Lingli, Li Kai, Wang Wenjun, Zhao Weiwei, Song Hui, Li Jianhua
Department of Biomaterials, School and Hospital of Stomatology, Cheeloo College of Medicine, Shandong University & Shandong Key Laboratory of Oral Tissue Regeneration & Shandong Engineering Research Center of Dental Materials and Oral Tissue Regeneration & Shandong Provincial Clinical Research Center for Oral Diseases, Jinan, 250012, China.
Department of Health Care (Department of General Dentistry Ⅱ), School and Hospital of Stomatology, Cheeloo College of Medicine, Shandong University & Shandong Key Laboratory of Oral Tissue Regeneration & Shandong Engineering Research Center of Dental Materials and Oral Tissue Regeneration & Shandong Provincial Clinical Research Center for Oral Diseases, Jinan, 250012, China.
Mater Today Bio. 2025 Aug 18;34:102213. doi: 10.1016/j.mtbio.2025.102213. eCollection 2025 Oct.
Periodontitis is an infectious disease caused by plaque-associated microorganisms. The condition is characterized by the activation of oxidative stress and immune responses, which contribute to tissue destruction. Carbon monoxide (CO)-based gas therapy, utilizing CO releasing molecules (CORMs), presents a promising therapeutic strategy; however, its efficacy is constrained by the short half-life and limited cellular uptake of CORMs. In this study, metal-phenolic networks (MPN) were employed as a carrier to stabilize CORMs via metal-ligand coordination, thereby forming a nanocomplex designated as CO@MPN. This nanocomplex demonstrated effective scavenging of reactive oxygen species (ROS) and exhibited ROS-responsive CO release. Following phagocytosis by macrophages, CO@MPN significantly decreased intracellular ROS levels, reduced the production of inflammatory factors in lipopolysaccharide (LPS)-stimulated macrophages, facilitated macrophage polarization towards the anti-inflammatory M2 phenotype, and activated heme oxygenase-1 (HO-1) to further attenuate inflammation. In murine models of experimental periodontitis, CO@MPN significantly inhibited inflammatory bone loss and exerted macrophage-regulating effects. The findings underscore the potential of ROS-responsive CO gas therapy as a promising strategy for the treatment of periodontitis and the management of other inflammatory diseases.
牙周炎是一种由牙菌斑相关微生物引起的感染性疾病。该病症的特征在于氧化应激和免疫反应的激活,这会导致组织破坏。利用一氧化碳释放分子(CORMs)的基于一氧化碳(CO)的气体疗法是一种很有前景的治疗策略;然而,其疗效受到CORMs半衰期短和细胞摄取有限的限制。在本研究中,金属-酚网络(MPN)被用作载体,通过金属-配体配位来稳定CORMs,从而形成一种名为CO@MPN的纳米复合物。这种纳米复合物表现出对活性氧(ROS)的有效清除,并呈现出ROS响应性的CO释放。在被巨噬细胞吞噬后,CO@MPN显著降低细胞内ROS水平,减少脂多糖(LPS)刺激的巨噬细胞中炎症因子的产生,促进巨噬细胞向抗炎M2表型极化,并激活血红素加氧酶-1(HO-1)以进一步减轻炎症。在实验性牙周炎的小鼠模型中,CO@MPN显著抑制炎症性骨质流失并发挥巨噬细胞调节作用。这些发现强调了ROS响应性CO气体疗法作为治疗牙周炎和管理其他炎症性疾病的一种有前景策略的潜力。