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中等强度 4mT 静磁场通过刺激链脲佐菌素处理的糖尿病大鼠的骨形成来防止骨结构恶化和骨强度降低。

Moderate-intensity 4mT static magnetic fields prevent bone architectural deterioration and strength reduction by stimulating bone formation in streptozotocin-treated diabetic rats.

机构信息

Department of Orthopedics, The Affiliated Hospital of Air Force Aviation Medicine Research Institute, Beijing 100089, China.

Department of Biomedical Engineering, Fourth Military Medical University, Xi'an, Shaanxi 710032, China.

出版信息

Bone. 2018 Feb;107:36-44. doi: 10.1016/j.bone.2017.10.024. Epub 2017 Oct 27.

DOI:10.1016/j.bone.2017.10.024
PMID:29111170
Abstract

Type 1 diabetes mellitus (T1DM) has been associated with deterioration of bone microarchitecture and strength, resulting in increased fracture risk. Substantial studies have revealed the capacity of moderate-intensity static magnetic fields (SMF) on promoting osteoblastogenesis in vitro and stimulating bone growth and bone regeneration in vivo, whereas it is unknown whether SMF can resist T1DM-associated osteopenia/osteoporosis. We herein investigated the potential effects of whole-body SMF exposure with 4mT on bone loss in streptozotocin-induced T1DM rats. We found that SMF exposure for 16weeks inhibited architectural deterioration of trabecular bone and cortical bone and mechanical strength reduction in T1DM rats, as evidenced by the MicroCT and 3-point bending findings. Our serum biochemical, bone histomorphometric and PCR results revealed that SMF induced higher serum osteocalcin, mineral apposition rate and osteoblast number of trabecular bone, and higher skeletal osteocalcin, BMP2 and Runx2 gene expression in T1DM rats, whereas SMF showed no significant alteration in serum CTX, skeletal osteoclast number, or osteoclastogenesis-related RANKL-RANK signaling gene expression. Together, our findings suggest that moderate SMF prevented bone architectural deterioration and strength reduction by inhibiting the reduction of bone formation in T1DM rats, and indicate that SMF might become a promising biophysical countermeasure for T1DM-related osteopenia/osteoporosis.

摘要

1 型糖尿病(T1DM)与骨微观结构和强度的恶化有关,导致骨折风险增加。大量研究表明,中等强度静磁场(SMF)具有促进体外成骨细胞生成和刺激体内骨生长和骨再生的能力,而 SMF 是否能抵抗 T1DM 相关的骨质疏松症尚不清楚。本研究旨在探讨全身 SMF 暴露(4mT)对链脲佐菌素诱导的 T1DM 大鼠骨丢失的潜在影响。我们发现,SMF 暴露 16 周可抑制 T1DM 大鼠的骨小梁和皮质骨结构恶化以及机械强度降低,这一结果通过 MicroCT 和三点弯曲试验得到证实。我们的血清生化、骨组织形态计量学和 PCR 结果表明,SMF 诱导 T1DM 大鼠血清骨钙素、矿化沉积率和骨小梁成骨细胞数量增加,骨骼骨钙素、BMP2 和 Runx2 基因表达增加,而 SMF 对血清 CTX、骨骼破骨细胞数量或破骨细胞生成相关 RANKL-RANK 信号基因表达无显著影响。总之,我们的研究结果表明,中等强度的 SMF 通过抑制 T1DM 大鼠骨形成减少来防止骨结构恶化和强度降低,这表明 SMF 可能成为治疗 T1DM 相关骨质疏松症的一种有前途的物理生物对策。

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