Chondrogenesis and subsequent osteogenesis of mesenchymal stem cells (MSCs) and angiogenesis at injured sites are crucial for bone fracture healing. Amygdalin, a cyanogenic glycoside compound derived from bitter apricot kernel, has been reported to inhibit IL-1β-induced chondrocyte degeneration and to stimulate blood circulation, suggesting a promising role of amygdalin in fracture healing. In this study, tibial fractures in C57BL/6 mice were treated with amygdalin. Fracture calluses were then harvested and subjected to radiographic, histological, and biomechanical testing, as well as angiography and gene expression analyses to evaluate fracture healing. The results showed that amygdalin treatment promoted bone fracture healing. Further experiments using MSC-specific transforming growth factor- (TGF-) β receptor 2 conditional knockout (KO) mice (Tgfbr2^Gli1-Cre) and C3H10 T1/2 murine mesenchymal progenitor cells showed that this effect was mediated through TGF-β/Smad signaling. We conclude that amygdalin could be used as an alternative treatment for bone fractures.

中文翻译：

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苦杏仁苷通过间质干细胞中的TGF-β/ Smad信号促进骨折愈合。

骨髓间充质干细胞（MSCs）的软骨形成和随后的成骨作用以及受伤部位的血管生成对于骨折愈合至关重要。苦杏仁苷，一种从苦杏仁仁中衍生的氰基糖苷化合物，据报道可抑制IL- 1β诱导的软骨细胞变性并刺激血液循环，表明苦杏仁苷在骨折愈合中具有有希望的作用。在这项研究中，使用苦杏仁苷治疗C57BL / 6小鼠的胫骨骨折。然后收获骨折老茧，并进行放射线照相，组织学和生物力学测试，以及血管造影和基因表达分析以评估骨折愈合。结果表明苦杏仁苷治疗促进骨折愈合。使用MSC特异性转化生长因子（TGF-）的进一步实验β受体2条件性敲除（KO）小鼠（Tgfbr2 ^Gli1-Cre）和C3H10 T1 / 2小鼠间充质祖细胞表明，这种作用是通过TGF- β / Smad信号传导介导的。我们得出结论，苦杏仁苷可以用作骨折的替代疗法。