BackgroundUltra‐high field magnetic resonance imaging (MRI) has obvious advantages in acquiring high‐resolution images. 7 T MRI has been clinically approved and 21.1 T MRI has also been tested on rodents.PurposeTo examine the effects of ultra‐high field on mice behavior and neuron activity.Study TypeProspective, animal model.Animal ModelNinety‐eight healthy C57BL/6 mice and 18 depression model mice.Field Strength11.1–33.0 T SMF (static magnetic field) for 1 hour and 7 T for 8 hours. Gradients were not on and no imaging sequence was used.AssessmentOpen field test, elevated plus maze, three‐chambered social test, Morris water maze, tail suspension test, sucrose preference test, blood routine, biochemistry examinations, enzyme‐linked immunosorbent assay, immunofluorescent assay.Statistical TestsThe normality of the data was assessed by Shapiro–Wilk test, followed by Student's t test or the Mann–Whitney U test for statistical significance. The statistical cut‐off line is P < 0.05.ResultsCompared to the sham group, healthy C57/6 mice spent more time in the center area (35.12 ± 4.034, increased by 47.19%) in open field test and improved novel index (0.6201 ± 0.02522, increased by 16.76%) in three‐chambered social test a few weeks after 1 hour 11.1–33.0 T SMF exposure. 7 T SMF exposure for 8 hours alleviated the depression state of depression mice, including less immobile time in tail suspension test (58.32% reduction) and higher sucrose preference (increased by 8.80%). Brain tissue analysis shows that 11.1–33.0 T and 7 T SMFs can increase oxytocin by 164.65% and 36.03%, respectively. Moreover, the c‐Fos level in hippocampus region was increased by 14.79%.Data Conclusion11.1–33.0 T SMFs exposure for 1 hour or 7 T SMF exposure for 8 hours did not have detrimental effects on healthy or depressed mice. Instead, these ultra‐high field SMFs have anti‐depressive potentials.Evidence Level1Technical EfficacyStage 1

Although some studies have shown that some static magnetic fields (SMFs) can promote wound healing in diabetic mice, it is not clear whether the other diabetes complications, such as liver disease and diabetic nephropathy, can also be alleviated. Here, we constructed two simple magnetic plates using neodymium permanent magnets to examine the comprehensive effects of moderate SMFs on genetically obese leptin receptor-deficient db/db diabetic mice. We found that although the blood glucose was not obviously reduced by these two SMF settings, both of the glycated serum protein (GSP) and malondialdehyde (MDA) levels were significantly decreased (Cohen’s d = 2.57–3.04). Moreover, the wound healing, liver lipid accumulation, and renal defects were all significantly improved by SMF treatment (Cohen’s d = 0.91–2.05). Wound tissue examination showed obvious nuclear factor erythroid 2-related factor 2 (NRF2) level decrease (Cohen’s d = 2.49–5.40) and Ki-67 level increase (Cohen’s d = 2.30–3.40), indicating decreased oxidative stress and increased cell proliferation. In vitro cellular studies with fibroblast NIH3T3 cells showed that SMFs could reduce high glucose-induced NRF2 nucleus translocation (Cohen’s d = 0.87–1.15) and cellular reactive oxygen species (ROS) elevation (Cohen’s d = 0.92), indicating decreased oxidative stress. Consequently, high glucose-induced impairments in cell vitality, proliferation, and migration were all improved by SMF treatment. Therefore, our results demonstrate that these simple SMF devices could effectively reduce oxidative stress in diabetic mice and may provide a cost-effective physical therapy strategy to alleviate multiple diabetic complications in the future.