title: Effect of remote ischemic post-conditioning on systemic inflammatory response and survival rate in lipopolysaccharide-induced systemic inflammation model.
abstract: BACKGROUND
  Remote ischemic preconditioning (RIPC) and postconditioning (RpostC) have protective effects on ischemia and reperfusion injury. The effects have been reported to activate heme oxygenase-1 (HO-1) and attenuate nuclear factor kappa B (NF-κB) and subsequently reduce systemic inflammation. Ischemic preconditioning prevented inflammatory responses by modulating HO-1 expression in endotoxic shock model. Therefore, we investigated whether RpostC could have protective effects on lipopolysaccharide (LPS)-induced systemic inflammation.
  
  
  METHODS
  The LPS-induced sepsis mice received LPS (20 mg/kg) intraperitoneally. Remote ischemic conditioning was induced with three 10-min ischemia/10-min reperfusion cycles of the right hind limbs using tourniquet before LPS injection (RIPC) or after LPS injection (RpostC). The effects of RIPC and RpostC were examined for the survival rate, serum cytokines, NF-κB, HO-1 and liver pathology in the LPS injected mice.
  
  
  RESULTS
  Survival rate within 120 hours significantly increased in the LPS injected and remote ischemic conditioned mice than in LPS only injected mice (60-65% vs 5%, respectively, p < 0.01). Tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β) and interleukin-6 (IL-6) increased markedly in the LPS only injected mice, however, remote ischemic conditioning suppressed the changes (p < 0.05). Interleukin-10 (IL-10) level was significantly higher in the LPS injected and RpostC treated mice than in the LPS only injected mice (p = 0.014). NF-κB activation was significantly attenuated (p < 0.05) and HO-1 levels were substantially higher in the LPS injected and remote ischemic conditioned mice than in the LPS only injected mice. Neutrophil infiltration was significantly attenuated in the LPS injected and remote ischemic conditioned mice than in the only LPS injected mice (p < 0.05).
  
  
  CONCLUSIONS
  RpostC attenuated inflammatory responses and improved survival outcomes of mice with LPS-induced systemic inflammation. The mechanism may be caused by modifying NF-κB mediated expression of cytokines.
authors.affiliation: Department of Anaesthesiology and Pain Medicine, Korea University College of Medicine, Ansan, Republic of Korea.
authors.forename: Yun-Hee
authors.initials: YH
authors.lastname: Kim
authors.affiliation: Division of Pulmonary, Sleep and Critical Care Medicine, Department of Internal Medicine, Korea University College of Medicine, Ansan, Republic of Korea.
authors.forename: Dae-Wui
authors.initials: DW
authors.lastname: Yoon
authors.affiliation: Division of Pulmonary, Sleep and Critical Care Medicine, Department of Internal Medicine, Korea University College of Medicine, Ansan, Republic of Korea.
authors.forename: Je-Hyeong
authors.initials: JH
authors.lastname: Kim
authors.affiliation: Department of Anaesthesiology and Pain Medicine, Dongguk University Ilsan Hospital, Ilsan, Republic of Korea.
authors.forename: Jeoung-Hyuk
authors.initials: JH
authors.lastname: Lee
authors.affiliation: Department of Anaesthesiology and Pain Medicine, Korea University College of Medicine, Seoul, Republic of Korea.
authors.forename: Choon-Hak
authors.initials: CH
authors.lastname: Lim
keywords: Remote ischemic postconditioning; Remote ischemic preconditioning; Systemic inflammation