title: Far infrared therapy inhibits vascular endothelial inflammation via the induction of heme oxygenase-1.
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.
  
  
  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.
authors.affiliation: Institute of Clinical Medicine, School of Medicine, National Yang-Ming University, Taipei, Taiwan.
authors.forename: Chih-Ching
authors.initials: CC
authors.lastname: Lin
authors.forename: Xiao-Ming
authors.initials: XM
authors.lastname: Liu
authors.forename: Kelly
authors.initials: K
authors.lastname: Peyton
authors.forename: Hong
authors.initials: H
authors.lastname: Wang
authors.forename: Wu-Chang
authors.initials: WC
authors.lastname: Yang
authors.forename: Shing-Jong
authors.initials: SJ
authors.lastname: Lin
authors.forename: William
authors.initials: W
authors.lastname: Durante
mesh_terms: D000368:Aged; D002478:Cells, Cultured; D042783:Endothelial Cells / Q000378:metabolism / Q000528:radiation effects; D004730:Endothelium, Vascular / Q000378:metabolism* / Q000528:radiation effects*; D004790:Enzyme Induction / Q000528:radiation effects; D005260:Female; D015870:Gene Expression / Q000528:radiation effects; D051547:Heme Oxygenase-1 / Q000096:biosynthesis* / Q000235:genetics; D006801:Humans; D007249:Inflammation / Q000201:enzymology / Q000235:genetics / Q000517:prevention & control*; D018836:Inflammation Mediators / Q000378:metabolism; D007259:Infrared Rays / Q000627:therapeutic use*; D018799:Intercellular Adhesion Molecule-1 / Q000096:biosynthesis; D008297:Male; D008875:Middle Aged; D009154:Mutation; D051267:NF-E2-Related Factor 2 / Q000235:genetics / Q000378:metabolism; D011401:Promoter Regions, Genetic; D011446:Prospective Studies; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D006435:Renal Dialysis; D014162:Transfection; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology; D019010:Vascular Cell Adhesion Molecule-1 / Q000096:biosynthesis
chemical_list: D018836:Inflammation Mediators; D051267:NF-E2-Related Factor 2; C495635:NFE2L2 protein, human; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D051547:Heme Oxygenase-1