title: Remote ischemic preconditioning prevents lipopolysaccharide-induced liver injury through inhibition of NF-κB activation in mice.
abstract: OBJECTIVE
  Remote ischemic preconditioning (RIPC) is a potent preconditioning stimulus that may confer subsequent protection to organs subjected to potentially lethal injury. The aim of this study was to investigate the effect of RIPC on nuclear factor (NF)-κB activation, tumor necrosis factor (TNF)-α release, and hepatic injury in lipopolysaccharide (LPS)-induced sepsis.
  
  
  METHODS
  This randomized experimental animal study was performed using 8-week-old mice weighing 35-40 g. Mice were randomized (n = 13 per group) to four groups. RIPC was induced with three 10-min cycles of hind limb ischemia by placing an elastic rubber band tourniquet on the proximal part of the limb, with each ischemia cycle followed by 10 min of reperfusion. The groups were treated as follows: (1) the control group received an injection of saline [intraperitoneally (i.p.)]; (2) the RIPC group was subjected to RIPC, followed immediately by an injection of saline (i.p.); (3) the LPS group received an injection of LPS (20 mg/kg, i.p.); (4) the RIPC/LPS group was subjected to RIPC, followed immediately by an injection of LPS (20 mg/kg, i.p.). TNF-α, NF-κB, and IκB-α levels, neutrophil accumulation, and microabscess formation in the liver were evaluated after LPS injection.
  
  
  RESULTS
  Among our treatment groups, RIPC significantly attenuated TNF-α release in response to endotoxin and inhibited NF-κB activation, neutrophil accumulation, and microabscess formation in the liver.
  
  
  CONCLUSIONS
  The results demonstrate that RIPC has protective effects in liver injury via attenuation of TNF-α production in LPS-induced sepsis. The suppressive effect on TNF-α production may be mediated through inhibition of NF-κB activation.
authors.affiliation: Department of Anesthesiology and Pain Medicine, College of Medicine, Korea University, No. 5 Anam-dong, Sungbuk-gu, Seoul, 136-705, Korea, may335@naver.com.
authors.forename: Hyeon Ju
authors.initials: HJ
authors.lastname: Shin
authors.forename: Nam Hee
authors.initials: NH
authors.lastname: Won
authors.forename: Hye Won
authors.initials: HW
authors.lastname: Lee
mesh_terms: D000818:Animals; D005121:Extremities; D020672:I-kappa B Proteins / Q000378:metabolism; D019194:Ischemic Preconditioning / Q000379:methods*; D008070:Lipopolysaccharides / Q000633:toxicity; D008099:Liver / Q000473:pathology; D008107:Liver Diseases / Q000209:etiology / Q000517:prevention & control*; D008297:Male; D051379:Mice; D000072000:NF-KappaB Inhibitor alpha; D016328:NF-kappa B / Q000378:metabolism*; D018805:Sepsis / Q000150:complications*; D014111:Tourniquets; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D020672:I-kappa B Proteins; D008070:Lipopolysaccharides; D016328:NF-kappa B; C000606205:Nfkbia protein, mouse; D014409:Tumor Necrosis Factor-alpha; D000072000:NF-KappaB Inhibitor alpha