Amygdalin Promotes Fracture Healing through TGF-beta/Smad Signaling in Mesenchymal Stem Cells
Amygdalin Promotes Fracture Healing through TGF-beta/Smad Signaling in Mesenchymal Stem Cells
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苦杏仁苷通过间充质干细胞中的 TGF-β/Smad 信号传导促进骨折愈合
DOI：
10.1155/2020/8811963
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发表时间：
2020
影响因子：
4.3
通讯作者：
Wang Pinger
中科院分区：
文献类型：
--
作者：
Ying Jun;Ge Qinwen;Hu Songfeng;Luo Cheng;Lu Fengyi;Yu Yikang;Xu Taotao;Lv Shuaijie;Zhang Lei;Shen Jie;Chen Di;Tong Peijian;Xiao Luwei;Li Ju;Jin Hongting;Wang Pinger
损伤部位间充质干细胞（MSCs）的软骨形成和随后的成骨以及血管生成对骨折愈合至关重要。苦杏仁苷是一种从苦杏仁中提取的氰苷类化合物，据报道，苦杏仁苷可以抑制il -1β诱导的软骨细胞变性并刺激血液循环，这表明苦杏仁苷在骨折愈合中有很好的作用。在本研究中，用苦杏仁苷治疗C57BL/6小鼠胫骨骨折。然后采集骨折痂，进行x线摄影、组织学和生物力学测试，以及血管造影和基因表达分析，以评估骨折愈合情况。结果表明，苦杏仁苷能促进骨折愈合。进一步使用msc特异性转化生长因子- (TGF-) β受体2条件敲除（KO）小鼠（Tgfbr2Gli1-Cre）和C3H10 T1/2小鼠间充质祖细胞进行的实验表明，这种作用是通过TGF-β/Smad信号介导的。我们认为苦杏仁苷可以作为骨折的替代治疗方法。
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 (Tgfbr2Gli1-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.