Extremely low frequency pulsed electromagnetic fields cause antioxidative defense mechanisms in human osteoblasts via induction of center dot O-2(-) and H2O2

作者：Ehnert, Sabrina^*; Fentz, Anne-Kristin; Schreiner, Anna; Birk, Johannes; Wilbrand, Benjamin; Ziegler, Patrick; Reumann, Marie K.; Wang, Hongbo; Falldorf, Karsten; Nussler, Andreas K.

来源：Scientific Reports, 2017, 7(1): 14544.

DOI：10.1038/s41598-017-14983-9

• LOTUS SEEDPOD PROCYANIDINS
• OXIDATIVE STRESS
• REACTIVE OXYGEN
• HIP FRACTURE
• DIFFERENTIATION
• MINERALIZATION
• PROLIFERATION
• ACTIVATION
• EXPOSURE
• ENZYMES

Recently, we identified a specific extremely low-frequency pulsed electromagnetic field (ELF-PEMF) that supports human osteoblast (hOBs) function in an ERK1/2-dependent manner, suggesting reactive oxygen species (ROS) being key regulators in this process. Thus, this study aimed at investigating how ELF-PEMF exposure can modulate hOBs function via ROS. Our results show that single exposure to ELF-PEMF induced ROS production in hOBs, without reducing intracellular glutathione. Repetitive exposure (>3) to ELF-PEMF however reduced ROS-levels, suggesting alterations in the cells antioxidative stress response. The main ROS induced by ELF-PEMF were center dot O-2(-) and H2O2, therefore expression/activity of antioxidative enzymes related to these ROS were further investigated. ELF-PEMF exposure induced expression of GPX3, SOD2, CAT and GSR on mRNA, protein and enzyme activity level. Scavenging center dot O-2(-) and H2O2 diminished the ELF-PEMF effect on hOBs AP activity and mineralization). Challenging the hOBs with low amounts of H2O2 on the other hand improved hOBs function. In summary, our data show that ELF-PEMF treatment favors differentiation of hOBs by producing nontoxic amounts of ROS, which induces antioxidative defense mechanisms in these cells. Thus, ELF-PEMF treatment might represent an interesting adjunct to conventional therapy supporting bone formation under oxidative stress conditions, e.g. during fracture healing.

• 出版日期2017-11-6
• 单位华中科技大学