State Key Laboratory of Oral Diseases & National Center for Stomatology & National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan, 610041, PR China.
Department of Oral and Maxillofacial Surgery, Affiliated Stomatological Hospital, Southwest Medical University, Luzhou, Sichuan, 646000, PR China.
Bone Res. 2024 Feb 29;12(1):14. doi: 10.1038/s41413-024-00319-7.
Diabetic osteoporosis (DOP) is a significant complication that poses continuous threat to the bone health of patients with diabetes; however, currently, there are no effective treatment strategies. In patients with diabetes, the increased levels of ferroptosis affect the osteogenic commitment and differentiation of bone mesenchymal stem cells (BMSCs), leading to significant skeletal changes. To address this issue, we aimed to target ferroptosis and propose a novel therapeutic approach for the treatment of DOP. We synthesized ferroptosis-suppressing nanoparticles, which could deliver curcumin, a natural compound, to the bone marrow using tetrahedral framework nucleic acid (tFNA). This delivery system demonstrated excellent curcumin bioavailability and stability, as well as synergistic properties with tFNA. Both in vitro and in vivo experiments revealed that nanoparticles could enhance mitochondrial function by activating the nuclear factor E2-related factor 2 (NRF2)/glutathione peroxidase 4 (GPX4) pathway, inhibiting ferroptosis, promoting the osteogenic differentiation of BMSCs in the diabetic microenvironment, reducing trabecular loss, and increasing bone formation. These findings suggest that curcumin-containing DNA tetrahedron-based ferroptosis-suppressing nanoparticles have a promising potential for the treatment of DOP and other ferroptosis-related diseases.
糖尿病性骨质疏松症(DOP)是一种严重的并发症,持续威胁着糖尿病患者的骨骼健康;然而,目前尚无有效的治疗策略。在糖尿病患者中,铁死亡水平的升高影响了骨髓间充质干细胞(BMSCs)的成骨承诺和分化,导致明显的骨骼变化。为了解决这个问题,我们旨在针对铁死亡,并提出一种治疗 DOP 的新方法。我们合成了铁死亡抑制纳米颗粒,该颗粒可以使用四面体框架核酸(tFNA)将姜黄素(一种天然化合物)递送至骨髓。该递药系统表现出优异的姜黄素生物利用度和稳定性,以及与 tFNA 的协同作用。体内外实验均表明,纳米颗粒可通过激活核因子 E2 相关因子 2(NRF2)/谷胱甘肽过氧化物酶 4(GPX4)通路增强线粒体功能,抑制铁死亡,促进糖尿病微环境中 BMSCs 的成骨分化,减少小梁丢失,增加骨形成。这些发现表明,基于 DNA 四面体的含姜黄素的铁死亡抑制纳米颗粒具有治疗 DOP 和其他铁死亡相关疾病的巨大潜力。