Static Magnetic Field Accelerates Diabetic Wound Healing by Facilitating Resolution of Inflammation

J Diabetes Res. 2019 Nov 30:2019:5641271. doi: 10.1155/2019/5641271. eCollection 2019.

Abstract

Impaired wound healing is commonly encountered in patients with diabetes mellitus, which may lead to severe outcomes such as amputation, if untreated timely. Macrophage plays a critical role in the healing process including the resolution phase. Although magnetic therapy is known to improve microcirculation, its effect on wound healing remains uncertain. In the present study, we found that 0.6 T static magnetic field (SMF) significantly accelerated wound closure and elevated reepithelialization and revascularization in diabetic mice. Notably, SMF promoted the wound healing by skewing the macrophage polarization towards M2 phenotype, thus facilitating the resolution of inflammation. In addition, SMF upregulated anti-inflammatory gene expression via activating STAT6 and suppressing STAT1 in macrophage. Taken together, our results indicate that SMF may be a promising adjuvant therapeutic tool for treating diabetic wounds.

MeSH terms

  • Animals
  • Cells, Cultured
  • Diabetic Angiopathies / genetics
  • Diabetic Angiopathies / metabolism
  • Diabetic Angiopathies / pathology
  • Diabetic Angiopathies / therapy*
  • Disease Models, Animal
  • Inflammation / metabolism
  • Inflammation / pathology
  • Inflammation / therapy*
  • Inflammation Mediators / metabolism
  • Macrophages, Peritoneal / metabolism
  • Macrophages, Peritoneal / pathology
  • Magnetic Field Therapy*
  • Male
  • Mice, Inbred Strains
  • Phenotype
  • STAT1 Transcription Factor / genetics
  • STAT1 Transcription Factor / metabolism
  • STAT6 Transcription Factor / genetics
  • STAT6 Transcription Factor / metabolism
  • Signal Transduction
  • Skin / metabolism
  • Skin / pathology*
  • Time Factors
  • Wound Healing*

Substances

  • Inflammation Mediators
  • STAT1 Transcription Factor
  • STAT6 Transcription Factor
  • Stat1 protein, mouse
  • Stat6 protein, mouse