本研究调查了四羧基酞菁铁 (FeTcPc) 对肿瘤坏死因子 α (TNF-α) 产生的活性和作用机制及其对实验性牙周炎的影响。用 FeTcPc 处理 RAW 264.7 巨噬细胞，并在 10 ℃下用脂多糖 (LPS) 激活。 ng/mL，并测量 TNF-α 水平以及核因子 kappa B (NF-κB) 激活。随后，将含有 1% FeTcPc 的口腔凝胶局部施用于具有牙周炎诱导结扎的小鼠的牙龈组织。对牙龈组织中的骨丢失以及 Tnfα、p65 (NF-κB) 和受体激活核因子 kappa B 配体 (Rankl) 的基因表达进行定量。最后，在大蜡螟幼虫中评估了 FeTcPc 的全身毒性。在活化的 RAW 264.7 巨噬细胞培养物中，100μM FeTcPc 减少了 TNF-α 的释放和 NF-κB 的激活。对于实验性牙周炎，局部使用含有 1% FeTcPc 的口腔凝胶可阻止牙槽骨流失。此外，1% FeTcPc 降低牙龈组织中 Tnfα、p65 (NF-κB) 和 Rankl 的表达。最后，以 1 至 1000mg/kg 的剂量施用 FeTcPc 不会引起大蜡螟的急性全身毒性。总体而言，我们证明了含有 FeTcPc 的口腔凝胶作为治疗溶骨性炎症性疾病（例如牙周炎）的潜力。 © 2024 约翰·威利

This study investigated the activity and mechanism of action of the iron tetracarboxyphthalocyanine (FeTcPc) on tumor necrosis factor alpha (TNF-α) production and its impact on experimental periodontitis.RAW 264.7 macrophages were treated with FeTcPc, activated with lipopolysaccharide (LPS) at 10 ng/mL, and the TNF-α levels were measured, as well as the nuclear factor kappa B (NF-κB) activation. Subsequently, a mouth gel containing 1% FeTcPc was topically administered to the gingival tissue of mice with periodontitis-induced ligatures. Bone loss and the gene expression of Tnfα, p65 (NF-κB), and receptor-activating nuclear factor kappa B ligand (Rankl) were quantified in gingival tissue. Finally, the systemic toxicity of FeTcPc was estimated in Galleria mellonella larvae.In an activated RAW 264.7 macrophage culture, 100 μM FeTcPc reduced TNF-α release and NF-κB activation. Regarding experimental periodontitis, topical application of mouth gel containing 1% FeTcPc blocked alveolar bone loss. Additionally, 1% FeTcPc reduced the expression of Tnfα, p65 (NF-κB), and Rankl in gingival tissue. Finally, administration FeTcPc at doses ranging from 1 to 1000 mg/kg did not cause acute systemic toxicity in G. mellonella.Overall, we demonstrated the potential of mouth gel containing FeTcPc as a therapeutic strategy for managing osteolytic inflammatory disorders, such as periodontitis.© 2024 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.