TY - JOUR
T1 - Amygdalin Promotes Fracture Healing through TGF- β /Smad Signaling in Mesenchymal Stem Cells
AU - Ying, Jun
AU - Ge, Qinwen
AU - Hu, Songfeng
AU - Luo, Cheng
AU - Lu, Fengyi
AU - Yu, Yikang
AU - Xu, Taotao
AU - Lv, Shuaijie
AU - Zhang, Lei
AU - Shen, Jie
AU - Chen, Di
AU - Tong, Peijian
AU - Xiao, Luwei
AU - Li, Ju
AU - Jin, Hongting
AU - Wang, Pinger
N1 - Publisher Copyright:
© 2020 Jun Ying et al.
PY - 2020
Y1 - 2020
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=85091700374&partnerID=8YFLogxK
U2 - 10.1155/2020/8811963
DO - 10.1155/2020/8811963
M3 - Article
C2 - 32963548
AN - SCOPUS:85091700374
SN - 1687-9678
VL - 2020
JO - Stem Cells International
JF - Stem Cells International
M1 - 8811963
ER -