Chondrocyte targeting gold nanoparticles protect growth plate against inflammatory damage by maintaining cartilage balance

被引:5
作者
Bai, Xue [1 ,4 ]
Sun, Hongyan [2 ]
Jia, Lina [2 ]
Xu, Junjie [2 ]
Zhang, Peng [2 ]
Zhang, Deyuan [2 ,3 ]
Gu, Yu [1 ,4 ]
Chen, Bo [2 ]
Feng, Lin [2 ,3 ]
机构
[1] Capital Med Univ, Sch Biomed Engn, Beijing 100069, Peoples R China
[2] Beihang Univ, Sch Mech Engn & Automat, Beijing 100191, Peoples R China
[3] Beihang Univ, Beijing Adv Innovat Ctr Biomed Engn, Beijing 100083, Peoples R China
[4] Beijing Key Lab Basic Res Clin Appl Biomech, Beijing, Peoples R China
关键词
Extracellular matrix; Gold nanoparticles; Growth plate; Inflammation-induced cartilage damage; OSTEOARTHRITIS; MATRIX; KNEE; INTERLEUKIN-1-BETA; LOCALIZATION; REGENERATION; PATHOGENESIS; DEGRADATION; EXPRESSION; MANAGEMENT;
D O I
10.1016/j.mtbio.2023.100795
中图分类号
R318 [生物医学工程];
学科分类号
0831 ;
摘要
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, approx-imately 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.
引用
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页数:13
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