RESULTS: Specifically, pPNP + TIIA@PFS elevates the concentration of the anti-aging protein Klotho and blocks the transmission of senescence signals to adjacent healthy chondrocytes, significantly mitigating chondrocyte senescence and enhancing cartilage integrity. Additionally, pPNP + TIIA@PFS recruit bone mesenchymal stem cells and directs their subsequent differentiation into chondrocytes, achieving satisfactory chondrogenesis. In surgically induced OA model rats, the application of pPNP + TIIA@PFS results in reduced osteophyte formation and attenuation of articular cartilage degeneration.
CONCLUSIONS: Overall, this study introduces a novel approach for the alleviation of OA progression, offering a foundation for potential clinical translation in OA therapy.
结果:具体来说,pPNP+TIIA@PFS提高抗衰老蛋白Klotho的浓度,并阻断衰老信号向相邻健康软骨细胞的传递,显着减轻软骨细胞衰老和增强软骨完整性。此外,pPNP+TIIA@PFS募集骨髓间充质干细胞并指导其随后分化为软骨细胞,实现令人满意的软骨形成。在手术诱导的OA模型大鼠中,pPNP+TIIA@PFS的应用导致骨赘形成减少和关节软骨退变的减轻。
结论:总体而言,这项研究介绍了一种新的方法来缓解OA的进展,为OA治疗中潜在的临床翻译奠定了基础。