A 0.2 T-0.4 T Static Magnetic Field Improves the Bone Quality of Mice Subjected to Hindlimb Unloading and Reloading Through the Dual Regulation of BMSCs via Iron Metabolism.

Abstract

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.