静磁场下铁元素通过调控线粒体氧化呼吸链影响破骨细胞分化功能

铁是人体必需微量元素，铁过载可通过增强线粒体活性氧生成，促进破骨细胞分化，从而导致骨质流失。静磁场对骨骼系统有正向的促进作用，具有骨吸收重要功能的破骨细胞对静磁场的响应少有研究。申请者研究发现静磁场影响破骨细胞的分化，引起细胞铁代谢水平变化，同时影响线粒体呼吸链复合体蛋白的表达。因此提出：铁元素通过调控线粒体氧化呼吸功能，引起破骨细胞活性氧水平改变，参与静磁场影响破骨细胞分化过程。. 本项目拟采用两种不同强度（亚磁和强磁）静磁场研究：①静磁场/铁元素对破骨细胞分化的影响；②静磁场/铁元素对破骨细胞铁元素含量与分布的影响；③静磁场/铁元素对线粒体氧化呼吸以及活性氧生成的影响。本研究将为深入理解磁场环境影响骨骼代谢的平衡机制提供新的实验依据，并为利用铁元素和磁场维护骨骼健康提供理论基础。

Iron is an essential trace element for human being. Iron overload promotes osteoclast differentiation via enhanced mitochondrial function and reactive oxygen species, which consequently induces osteoporosis. Certain static magnetic fields (SMFs) have positive effects on skeleton system. However, there are few studies focusing on the responses of osteoclasts to SMF. Our recent research showed that SMF can modulate osteoclast differentiation, with the altered level of iron metabolism. Meanwhile, expressions of mitochondria complex I-V proteins are influenced. Basing on this, we propose a hypothesis that the static magnetic fields induce osteoclast differentiation via iron-mediated mitochondrial respiratory chain..We will carry out following investigations by using two types of SMFs differing in intensities (hypo and high SMF): ①influence of SMFs/iron on osteoclast differentiation; ②influence of SMFs/iron on the content and distribution of iron in osteoclast; ③influence of SMF/iron on mitochondrial respiratory chain and yields of reactive oxygen species. The objective of this research is to provide new experimental evidence for better understanding the balance of bone metabolism under SMFs and provide some theoretical basis for maintenance of bone health by using iron and SMFs.