Abstract
Objective The present study intends to investigate the effects and underlying molecular mechanism of Qigu Capsule (QG) on fracture healing in mice with osteoporosis. Methods Ten-week-old female C57BL/6 mice were ovariectomized and three weeks later were evaluated for successful modeling. Then, all mice were prepared into models of transverse fracture in the right middle femoral shaft. Mice were treated daily using a gavage with normal saline (the NS group), Qigu Capsule (the QG group), or alendronate (the ALN group) postoperatively. Fracture callus tissues were collected and analyzed by X-ray, micro-CT, western blot (WB), and transmission electron microscope (TEM) on postoperation Day 14 (POD14), POD28, and POD42. Results (1) X-ray results showed that on POD14, the QG group had the fracture healing score significantly higher than the NS and ALN groups, and on POD28, it had the fracture healing score higher than the NS group, suggesting that QG could promote fracture healing. (2) Micro-CT results showed that on POD14, the QG group had tissue bone density (TMD) significantly higher than the NS and ALN groups, and on POD28 and POD42, it had bone volume fraction, trabecular number, and TMD significantly higher than the NS group. (3) WB results showed that, compared with the NS group, the QG group had significantly increased expression of nuclear factor kappa-B (NF-κB), hypoxia-inducible factor-1α (HIF-1α), bone alkaline phosphatase (BALP), runt-related transcription factor 2 (Runx2), bone Gla protein (BGP) and collagen Iα1 (COLIα1) on POD14, significantly increased expression of NF-κB, HIF-1α, BALP and COLIα1 on POD28, and significantly increased expression of NF-κB, HIF-1α, and Runx2 on POD42. (4) TEM scanning results showed that, compared with the NS and ALN groups, the QG group had significantly increased numbers of autophagic vacuoles (AVs) in osteocytes on POD14, POD28, and POD42. Conclusion QG could accelerate osteoporotic fracture healing by promoting bone formation and osteocyte autophagy, possibly through upregulating the NF-κB/HIF-1α signaling pathway.
Highlights
With the population aging, fragility fracture has become a worldwide disease [1]
Fragility fracture has become a worldwide disease [1]. It is the most serious consequence of osteoporosis, a systemic skeletal disease characterized by low bone mass and microarchitectural deterioration of bone tissue that cause an increase in bone fragility [2]
Evidence-Based Complementary and Alternative Medicine. It has been proposed in relevant guidelines that the prevention and treatment of fragility fracture should focus on intervention of the primary disease, enhancement of bone mineral density (BMD), and prevention of refracture [1]
Summary
Fragility fracture has become a worldwide disease [1]. Studies have shown that osteoporosis may delay fracture healing and reduce the biochemical properties of bone, and the risk of bone nonunion and death after fragility fracture is increasing [3,4,5]. It has been proposed in relevant guidelines that the prevention and treatment of fragility fracture should focus on intervention of the primary disease, enhancement of bone mineral density (BMD), and prevention of refracture [1]. Traditional Chinese medicine (TCM) compounds for kidney reinforcing have confirmed efficacy in preventing and treating fragility fracture, and they can increase BMD and improve bone metabolism and bone turnovermarkers in patients with osteoporosis [9]. Animal experiments demonstrate that TCM compounds for kidney reinforcing act against osteoporosis significantly, the mechanism of which involves multiple regulatory pathways [10]
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