Bai Xue, Sun Hongyan, Jia Lina, Xu Junjie, Zhang Peng, Zhang Deyuan, Gu Yu, Chen Bo, Feng Lin
School of Biomedical Engineering, Capital Medical University, Beijing, 100069, China.
Beijing Key Laboratory of Basic Research in Clinical Applied Biomechanics, China.
Mater Today Bio. 2023 Sep 14;23:100795. doi: 10.1016/j.mtbio.2023.100795. eCollection 2023 Dec.
Cartilage destruction caused by inflammation is a clinical challenge. Many studies have investigated cartilage destruction in adults, but little research was conducted on children. In this study, the protective effect of gold nanoparticles (AuNPs) on the cartilage of children was realized by counteracting chondrocyte apoptosis and extracellular matrix (ECM) degradation in a young mouse model of lipopolysaccharide (LPS)-induced growth plate (GP) cartilage damage. Initially, engineered AuNPs can be efficiently absorbed by chondrocytes, approximately 20 times the amount absorbed by macrophages, resulting in a 29% ± 0.05% increase in chondrocyte viability. Then, AuNPs exposure significantly reduced the release of inflammatory cytokines and secretion of ECM degradation factors induced by LPS. Subsequently, AuNPs were applied to resist LPS-induced cartilage destruction in young mice. AuNPs inhibited the formation of gaps, without chondrocytes and extracellular matrix, between the proliferative and hypertrophy zones of the GP cartilage, and the gaps were noticeable in the LPS group. This finding can be attributed to the capability of AuNPs to reduce the LPS-induced apoptosis rate of mouse chondrocytes by 72.38% and the LPS-induced ECM degradation rate by 70.89%. Further analysis demonstrated that remission is partly due to AuNPs' role in maintaining the balance of catabolic and anabolic factors in the ECM. Altogether, these findings indicate that AuNPs can partially protect the cartilage of children from inflammatory damage by suppressing chondrocyte apoptosis and ECM degradation.
炎症引起的软骨破坏是一项临床挑战。许多研究调查了成人的软骨破坏情况，但针对儿童的研究较少。在本研究中，通过在脂多糖（LPS）诱导的生长板（GP）软骨损伤的幼鼠模型中抵消软骨细胞凋亡和细胞外基质（ECM）降解，实现了金纳米颗粒（AuNPs）对儿童软骨的保护作用。最初，工程化的AuNPs能够被软骨细胞有效吸收，吸收量约为巨噬细胞的20倍，使软骨细胞活力提高了29%±0.05%。然后，AuNPs暴露显著减少了LPS诱导的炎性细胞因子释放和ECM降解因子的分泌。随后，将AuNPs应用于抵抗幼鼠LPS诱导的软骨破坏。AuNPs抑制了GP软骨增殖区和肥大区之间无软骨细胞和细胞外基质的间隙形成，而在LPS组中这些间隙很明显。这一发现可归因于AuNPs能够将LPS诱导的小鼠软骨细胞凋亡率降低72.38%，并将LPS诱导的ECM降解率降低70.89%。进一步分析表明，缓解部分归因于AuNPs在维持ECM中分解代谢和合成代谢因子平衡方面的作用。总之，这些发现表明AuNPs可以通过抑制软骨细胞凋亡和ECM降解，部分保护儿童软骨免受炎性损伤。
