Wang Jianping, Zhen Chenxiao, Zhang Gejing, Yang Zhouqi, Shang Peng
School of Life Sciences, Northwestern Polytechnical University, Xi'an 710072, China.
Key Laboratory for Space Bioscience and Biotechnology, Institute of Special Environmental Biophysics, School of Life Sciences, Northwestern Polytechnical University, Xi'an 710072, China.
Int J Mol Sci. 2024 Dec 6;25(23):13136. doi: 10.3390/ijms252313136.
Osteoporosis is the most prevalent metabolic bone disease, especially when aggravated by aging and long-term bed rest of various causes and also when coupled with astronauts' longer missions in space. Research on the use of static magnetic fields (SMFs) has been progressing as a noninvasive method for osteoporosis due to the complexity of the disease, the inconsistency of the effects of SMFs, and the ambiguity of the mechanism. This paper studied the effects of mice subjected to hindlimb unloading (UL, HLU) and reloading by the 0.2 T-0.4 T static magnetic field (MMF). Primary bone marrow mesenchymal stem cells (BMSCs) were extracted to explore the mechanism. Eight-week-old male C57BL/6 mice were used as an osteoporosis model by HLU for four weeks. The HLU recovery period (reloading, RL) was carried out on all FVEs and recovered in the geomagnetic field (45-64 μT, GMF) and MMF, respectively, for 12 h/d for another 4 weeks. The tibia and femur of mice were taken; also, the primary BMSCs were extracted. MMF promoted the recovery of mechanical properties after HLU, increased the number of osteoblasts, and decreased the number of adipocytes in the bone marrow. MMF decreased the total iron content and promoted the total calcium content in the tibia. In vitro experiments showed that MMF promoted the osteogenic differentiation of BMSCs and inhibited adipogenic differentiation, which is related to iron metabolism, the Wnt/β-catenin pathway, and the PPARγ pathway. MMF accelerated the improvement in bone metabolism and iron metabolism in RL mice to a certain extent, which improved the bone quality of mice. MMF mainly promoted osteogenic differentiation and reduced the adipogenic differentiation of BMSCs, which provides a reliable research direction and transformation basis for the osteoporosis of elderly, bedridden patients and astronauts.
骨质疏松症是最常见的代谢性骨病，尤其是在因衰老、各种原因导致的长期卧床休息而加重时，以及在宇航员执行更长时间的太空任务时。由于该疾病的复杂性、静磁场（SMFs）作用效果的不一致性以及作用机制的模糊性，作为一种治疗骨质疏松症的非侵入性方法，对静磁场的研究一直在进行。本文研究了0.2 T - 0.4 T静磁场（MMF）对后肢卸载（UL，HLU）和再加载小鼠的影响。提取原代骨髓间充质干细胞（BMSCs）以探究其机制。8周龄雄性C57BL/6小鼠通过后肢卸载4周作为骨质疏松模型。对所有后肢卸载的小鼠进行恢复期（再加载，RL），分别在地磁场（45 - 64 μT，GMF）和静磁场中恢复，每天12小时，持续4周。取小鼠的胫骨和股骨；同时，提取原代BMSCs。静磁场促进了后肢卸载后力学性能的恢复，增加了成骨细胞数量，并减少了骨髓中脂肪细胞的数量。静磁场降低了胫骨中的总铁含量并促进了总钙含量。体外实验表明，静磁场促进了BMSCs的成骨分化并抑制了脂肪生成分化，这与铁代谢、Wnt/β - 连环蛋白通路和PPARγ通路有关。静磁场在一定程度上加速了再加载小鼠骨代谢和铁代谢的改善，从而提高了小鼠的骨质量。静磁场主要促进了BMSCs的成骨分化并减少了其脂肪生成分化，这为老年、卧床患者和宇航员的骨质疏松症提供了可靠的研究方向和转化依据。
