Recently, as our population increasingly ages with more pressure on bone and cartilage diseases, bone/cartilage tissue engineering (TE) have emerged as a potential alternative therapeutic technique accompanied by the rapid development of materials science and engineering. The key part to fulfill the goal of reconstructing impaired or damaged tissues lies in the rational design and synthesis of therapeutic agents in TE. Gold nanomaterials, especially gold nanoparticles (AuNPs), have shown the fascinating feasibility to treat a wide variety of diseases due to their excellent characteristics such as easy synthesis, controllable size, specific surface plasmon resonance and superior biocompatibility. Therefore, the comprehensive applications of gold nanomaterials in bone and cartilage TE have attracted enormous attention. This review will focus on the biomedical applications and molecular mechanism of gold nanomaterials in bone and cartilage TE. In addition, the types and cellular uptake process of gold nanomaterials are highlighted. Finally, the current challenges and future directions are indicated.
Epidural fibrosis (EF)-induced failed back surgery syndrome (FBSS) in patients post-laminectomy remains a medical challenge. Although the scarring mechanisms remain unclear, the majority of aetiological studies have reported fibroblast dysfunction. Honokiol, the major bioactive constituent of the magnolia tree, exerts a variety of pharmacological effects, including anti-proliferative and anti-fibrotic effects, on various cell types. The present study investigated whether honokiol attenuates EF progression.
In vitro
, it was found that honokiol inhibited excessive fibroblast proliferation induced by transforming growth factor-β1 (TGF-β1) and the synthesis of extracellular matrix (ECM) components, including fibro-nectin and type I collagen, in a dose-dependent manner. These effects were attributed to the ability of honokiol to suppress the activity of connective tissue growth factor (CTGF), which is indispensable for the progression of fibrosis. Mechanistically, honokiol attenuated the TGF-β1-induced activation of the Smad2/3 and mitogen-activated protein kinase (MAPK) signalling pathways in fibroblasts.
In vivo
, honokiol reduced the proliferation of fibroblasts and the synthesis of ECM components, thus ameliorating EF in a rat model post-laminectomy. Taken together, these preclinical findings suggest that honokiol deserves further consideration as a candidate therapeutic agent for EF.
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