Zhang Jian, Ding Chong, Meng Xiaofeng, Shang Peng
a School of Radiation Medicine and Protection , Medical College of Soochow University , Suzhou , China.
b Collaborative Innovation Center of Radiation Medicine of Jiangsu Higher Education Institutions , Suzhou , China.
Electromagn Biol Med. 2018;37(1):23-34. doi: 10.1080/15368378.2017.1414057. Epub 2017 Dec 13.
Nitric oxide (NO) is involved in osteoclast differentiation. Our previous studies showed that static magnetic fields (SMFs) could affect osteoclast differentiation. The inhibitory effects of 16 T of high SMF (HiMF) on osteoclast differentiation was correlated with increased production of NO. We raised the hypothesis that NO mediated the regulatory role of SMFs on osteoclast formation. In this study, 500 nT of hypomagnetic field (HyMF), 0.2 T of moderate SMF (MMF) and 16 T of high SMF (HiMF) were utilized as SMF treatment. Under 16 T, osteoclast formation was markedly decreased with enhanced NO synthase (NOS) activity, thus producing a high level of NO. When treated with NOS inhibitor N-Nitro-L-Arginine Methyl Ester (L-NAME), NO production could be inhibited, and osteoclast formation was restored to control group level in a concentration-dependent manner. However, 500 nT and 0.2 T increased osteoclast formation with decreased NOS activity and NO production. When treated with NOS substrate L-Arginine (L-Arg) or NO donor sodium nitroprusside (SNP), the NO level in the culture medium was obviously elevated, thus inhibiting osteoclast differentiation in a concentration-dependent manner under 500 nT or 0.2 T. Therefore, these findings indicate that NO mediates the regulatory role of SMF on osteoclast formation.
一氧化氮（NO）参与破骨细胞分化。我们之前的研究表明，静磁场（SMF）可影响破骨细胞分化。16T的高静磁场（HiMF）对破骨细胞分化的抑制作用与NO生成增加相关。我们提出假设，即NO介导了SMF对破骨细胞形成的调节作用。在本研究中，使用500nT的低磁场（HyMF）、0.2T的中等静磁场（MMF）和16T的高静磁场（HiMF）作为SMF处理。在16T下，破骨细胞形成明显减少，同时一氧化氮合酶（NOS）活性增强，从而产生高水平的NO。用NOS抑制剂N-硝基-L-精氨酸甲酯（L-NAME）处理时，NO生成可被抑制，破骨细胞形成以浓度依赖的方式恢复到对照组水平。然而，500nT和0.2T使破骨细胞形成增加，同时NOS活性和NO生成减少。用NOS底物L-精氨酸（L-Arg）或NO供体硝普钠（SNP）处理时，培养基中的NO水平明显升高，从而在500nT或0.2T下以浓度依赖的方式抑制破骨细胞分化。因此，这些发现表明NO介导了SMF对破骨细胞形成的调节作用。
