Bai Xue, Chen Dixiao, Dai Yuguo, Liang Shuzhang, Song Bin, Guo Jiurong, Dai Bofang, Zhang Deyuan, Feng Lin
School of Mechanical Engineering & Automation, Beihang University, Beijing, China.
School of Mechanical Engineering & Automation, Beihang University, Beijing, China; Beijing Advanced Innovation Center for Biomedical Engineering, Beihang University, Beijing, China.
Nanomedicine. 2021 Nov;38:102457. doi: 10.1016/j.nano.2021.102457. Epub 2021 Aug 13.
The prevention of fractures induced by inflammatory bone disease remains a clinical challenge. This is because of a lack of bone formation to fill in the bone defects, which are believed to be due in part to persistent inflammation caused by the imbalance of M1 over M2 macrophages. In this study, gold nanoparticles (AuNPs) were synthesized to shift the balance of macrophages at the site of bone damage to improve osteanagenesis in a mouse model of LPS-induced inflammatory bone erosion. Specifically, the AuNPs treatment improved bone structure and increased bone mineral density (BMD) by ~14% compared with model group. Macrophages recruited by LPS treatment were reduced by ~11% after AuNPs injection. Compared to LPS treatment only, the percentage of M2 macrophages increased threefold by AuNPs, while the proportion of M1 macrophages decreased by 59%. This promoted the regeneration of bone matrix proteins in the bone defect site, which finally leads to increased bone mass and improved bone structure in model mice. These data suggest that AuNPs could be a novel candidate therapeutic for inflammatory bone disease rather than a drug carrier.
预防炎症性骨病引起的骨折仍然是一项临床挑战。这是因为缺乏骨形成来填充骨缺损，据信部分原因是M1巨噬细胞与M2巨噬细胞失衡导致的持续炎症。在本研究中，合成了金纳米颗粒（AuNPs），以改变骨损伤部位巨噬细胞的平衡，从而在脂多糖（LPS）诱导的炎症性骨侵蚀小鼠模型中改善骨生成。具体而言，与模型组相比，AuNPs治疗改善了骨结构，并使骨矿物质密度（BMD）增加了约14%。注射AuNPs后，LPS治疗招募的巨噬细胞减少了约11%。与仅进行LPS治疗相比，AuNPs使M2巨噬细胞的百分比增加了两倍，而M1巨噬细胞的比例下降了59%。这促进了骨缺损部位骨基质蛋白的再生，最终导致模型小鼠骨量增加和骨结构改善。这些数据表明，AuNPs可能是炎症性骨病的一种新型候选治疗方法，而非药物载体。
