Department of Bone & Joint Surgery, Peking University Shenzhen Hospital, Shenzhen 518036, China.
National & Local Joint Engineering Research Center of Orthopaedic Biomaterials, Peking University Shenzhen Hospital, Shenzhen 518036, China.
ACS Biomater Sci Eng. 2024 Sep 9;10(9):5796-5806. doi: 10.1021/acsbiomaterials.4c00713. Epub 2024 Aug 19.
Cartilage defects caused by joint diseases are difficult to treat clinically. Tissue engineering materials provide a new means to promote the repair of cartilage defects. The purpose of this study is to design a novel scaffold of porous magnesium alloy loaded with icariin and sustained release in order to explore the effect and possible mechanism of this scaffold in repairing SD rat knee articular cartilage defect. We constructed a novel type of icariin/porous magnesium alloy scaffold, observed the structure of the scaffold by electron microscope, detected the drug release of icariin in the scaffold and the biological safety, and established an animal model of cartilage defect in the femoral intercondylar fossa of the knee joint in rats; the scaffold was placed in the defect. After 12 weeks of repair, the rat knee articular cartilage repair was evaluated by gross specimens and micro-CT, HE, safranin O-fast green, and toluidine blue staining combined with the modified Mankin's score. The protein expressions of the Wnt/β-catenin signaling pathway-related factors (β-catenin, Wnt5a, Wnt1, sFRP1) and chondrogenic differentiation-related factors (Sox9, Aggrecan, Col2α1) were detected by immunohistochemical staining. We found that the novel scaffold of icariin/porous magnesium alloy can release icariin slowly and has biosafety in rats. Compared with other groups, icariin/porous magnesium alloy can significantly promote the repair of cartilage defects and the expressions of β-catenin, Wnt5a, Wnt1, Sox9, Aggrecan, and Col2α1 ( < 0.05). This novel scaffold can promote the repair of rat knee cartilage defects, and this process may be achieved by activating the Wnt/β-catenin signaling pathway.
关节疾病引起的软骨缺损临床上难以治疗。组织工程材料为促进软骨缺损修复提供了新手段。本研究旨在设计一种新型载淫羊藿苷多孔镁合金支架并实现其缓慢释放,以探讨该支架修复 SD 大鼠膝关节软骨缺损的效果及可能机制。我们构建了一种新型的淫羊藿苷/多孔镁合金支架,通过电子显微镜观察支架的结构,检测支架中淫羊藿苷的药物释放及生物安全性,建立大鼠膝关节股骨髁间窝软骨缺损动物模型,将支架置于缺损处。修复 12 周后,通过大体标本和 micro-CT、HE、番红 O-快绿、甲苯胺蓝染色结合改良 Mankin 评分评估大鼠膝关节软骨修复情况,免疫组化染色检测 Wnt/β-catenin 信号通路相关因子(β-catenin、Wnt5a、Wnt1、sFRP1)和软骨分化相关因子(Sox9、Aggrecan、Col2α1)的蛋白表达。结果发现,新型的淫羊藿苷/多孔镁合金支架能够缓慢释放淫羊藿苷,且在大鼠体内具有生物安全性。与其他组相比,淫羊藿苷/多孔镁合金支架能更显著地促进软骨缺损修复,以及β-catenin、Wnt5a、Wnt1、Sox9、Aggrecan、Col2α1 的表达(<0.05)。新型支架能够促进大鼠膝关节软骨缺损的修复,该过程可能是通过激活 Wnt/β-catenin 信号通路实现的。