作者
Zhenhua Song,Wei Xie,Siyi Zhu,Jinjing Pan,Lu-Yao Zhou,Chengqi He
摘要
Objective: Ovariectomized mice were used to simulate the symptoms of postmenopausal women with osteoporosis, and observe the effects of PEMF treatment on expression of Osx, Ocn, TRAP, and CTSK in ovariectomized mice. Methods: Thirty-week-old wild-type C57BL/6 mice were randomly divided into three groups (n=10, each group): sham operation group, ovariectomy (OVX) group, and PEMF group. Mice in the sham group underwent sham ovariectomy, while mice in the remaining two groups were ovariectomized. On postoperative day two, mice in the PEMF treatment group received PEMF treatment at a frequency of 8 Hz and an intensity of 3.8 mT for one hour daily for four weeks. At the same time, mice in the remaining two groups were placed in the PEMF treatment area under power-down state daily, similar to that in the PEMF group. After four weeks, all relevant indicators were tested. Results: (1) Compared with mice in the sham group, the number of trabecular bones significantly decreased, the thickness of the trabecular bone became thinner, the number of osteoclasts significantly increased, the gene expression of Osx and Ocn significantly decreased, and the gene expression of TRAP and CTSK significantly increased in the OVX group (P<0.01). (2) Compared with the blank controls without operation, the number of osteoblasts increased in the PEMF group. (3) Compared with the OVX group, the number of osteoclasts significantly decreased, the expression of Osx and Ocn significantly increased, and the gene expression of TRAP and CTSK significantly decreased in the PEMF group (P<0.01). Conclusion: PEMF treatment can significantly promote bone formation, which may be realized through inhibition of osteoclast formation, achieving bone morphological protection. PEMFs can significantly upregulate Osx and Ocn osteogenesis-related genes, which affect bone formation, and downregulate TRAP and CTSK osteoclast-related genes, which affect bone resorption. PEMFs may be used to treat postmenopausal osteoporosis by regulating Osx, Ocn, TRAP, and CTSK gene expression.