Magnetic Field Exposure Modulates the Anti-Inflammatory Efficiency of Minocycline in Rats with Peripheral Acute Inflammation.

Background and Objective Microglial activation in spinal cord is key contributor and its inhibition by Minocycline (MCN) can result in anti-inflammatory actions. Effect of pulsed magnetic field (PMF) in living system is a very complex process and many biological and cellular processes can play key roles. In this study aimed to reveal the roles of PMF exposure on anti-inflammatory potentials of MCN treatment by evaluating the inflammatory profiles of either inflamed site or spinal cord. Methods In this study, we investigated the anti-inflammatory effects of PMF, MCN or their combination treatments in rats with carrageenan (CG)-induced peripheral inflammation by examining the cardinal signs, hyperalgesia, allodynia, edema and fever. The levels of various inflammation markers (tumor necrosis factor-α), interleukin (IL)-1β, IL-6, IL-17, IL-4, IL-10, C-C motif chemokine ligand3 (CCL3), C-X-C motif chemokine ligand1 and myeloperoxidase were also measured in paw and spinal cord tissues. Results CG induced inflammation caused edema, fever, and hypersensitivities. MNC or PMF treatments ameliorated these responses by suppressing pro-inflammatory markers in both inflamed paw and spinal cord. Although anti-hypersensitive, anti-edematous and anti-pyretic actions of MCN or PMF, in combined treatments PMF exposure decreased the anti-hyperalgesic and anti-allodynic actions of MCN treatment. These may be associated with decreases in IL-4 and IL-10 levels and an increase in CCL3 level of spinal cord tissues. Conclusion Present findings support that MCN or PMF has anti-inflammatory properties duo to the down-regulating central microglial and/or peripheral inflammatory markers. Our data showed here, for the first time, PMF exposure may suppress the anti-hypersensitive actions of MCN by modulating microglia function/phenotype and microglial markers.