Abstract
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.
Highlights
Bone fractures, mainly caused by traumatic incidents and medical conditions, including osteoporosis, are a growing global health burden currently affecting millions of people [1, 2]
To assess the effects of amygdalin on fracture healing, mice were treated with phosphate-buffered saline (PBS) or amygdalin (0.5 mg/kg/day)
Our study demonstrated that treatment with amygdalin promotes fracture healing mainly through transforming growth factor- (TGF-)β/Smad signaling in mesenchymal stem cells (MSCs)
Summary
Mainly caused by traumatic incidents and medical conditions, including osteoporosis, are a growing global health burden currently affecting millions of people [1, 2]. Mesenchymal stem cells (MSCs) can migrate to the fracture site and differentiate into chondrocytes, which form a cartilaginous soft callus. This primary callus is subsequently surrounded by new bone material produced by osteoblasts in the perichondrium and permeated with blood vessels. The promotion of chondrogenesis/osteogenesis and angiogenesis can accelerate fracture healing. The origin of MSCs is not fully understood, but the recruitment, proliferation, and differentiation of these cells are indispensable for fracture healing [11]. Amygdalin has been implicated in the regulation of transforming growth factor- (TGF-) β/Smad signaling [18], which has a fundamental regulatory function for bone homeostasis [19, 20]. We hypothesized that amygdalin can promote bone fracture healing through TGF-β/Smad signaling
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