Far infrared therapy inhibits vascular endothelial inflammation via the induction of heme oxygenase-1

Arterioscler Thromb Vasc Biol. 2008 Apr;28(4):739-45. doi: 10.1161/ATVBAHA.107.160085. Epub 2008 Jan 17.

Abstract

Objective: Survival of arteriovenous fistulas (AVFs) in hemodialysis patients is associated with both far infrared (FIR) therapy and length polymorphisms of the heme oxygenase-1 (HO-1) promoter. In this study, we evaluated whether there is an interaction between FIR radiation and HO-1 in regulating vascular inflammation.

Methods and results: Treatment of cultured human umbilical vein endothelial cells (ECs) with FIR radiation stimulated HO-1 protein, mRNA, and promoter activity. HO-1 induction was dependent on the activation of the antioxidant responsive element/NF-E2-related factor-2 complex, and was likely a consequence of heat stress. FIR radiation also inhibited tumor necrosis factor (TNF)-alpha-mediated expression of E-selectin, vascular cell adhesion molecule-1, intercellular cell adhesion molecule-1, monocyte chemoattractant protein-1, interleukin-8, and the cytokine-mediated adhesion of monocytes to ECs. The antiinflammatory action of FIR was mimicked by bilirubin, and was reversed by the HO inhibitor, tin protoporphyrin-IX, or by the selective knockdown of HO-1. Finally, the antiinflammatory effect of FIR was also observed in patients undergoing hemodialysis.

Conclusions: These results demonstrate that FIR therapy exerts a potent antiinflammatory effect via the induction of HO-1. The ability of FIR therapy to inhibit inflammation may play a critical role in preserving blood flow and patency of AVFs in hemodialysis patients.

Publication types

  • Randomized Controlled Trial
  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Cells, Cultured
  • Endothelial Cells / metabolism
  • Endothelial Cells / radiation effects
  • Endothelium, Vascular / metabolism*
  • Endothelium, Vascular / radiation effects*
  • Enzyme Induction / radiation effects
  • Female
  • Gene Expression / radiation effects
  • Heme Oxygenase-1 / biosynthesis*
  • Heme Oxygenase-1 / genetics
  • Humans
  • Inflammation / enzymology
  • Inflammation / genetics
  • Inflammation / prevention & control*
  • Inflammation Mediators / metabolism
  • Infrared Rays / therapeutic use*
  • Intercellular Adhesion Molecule-1 / biosynthesis
  • Male
  • Middle Aged
  • Mutation
  • NF-E2-Related Factor 2 / genetics
  • NF-E2-Related Factor 2 / metabolism
  • Promoter Regions, Genetic
  • Prospective Studies
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Renal Dialysis
  • Transfection
  • Tumor Necrosis Factor-alpha / pharmacology
  • Vascular Cell Adhesion Molecule-1 / biosynthesis

Substances

  • Inflammation Mediators
  • NF-E2-Related Factor 2
  • NFE2L2 protein, human
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha
  • Vascular Cell Adhesion Molecule-1
  • Intercellular Adhesion Molecule-1
  • Heme Oxygenase-1