Effect of remote ischemic post-conditioning on systemic inflammatory response and survival rate in lipopolysaccharide-induced systemic inflammation model

详细信息    查看全文

• 作者：Yun-Hee Kim ; Dae-Wui Yoon ; Je-Hyeong Kim ; Jeoung-Hyuk Lee…
• 关键词：Remote ischemic preconditioning ; Remote ischemic postconditioning ; Systemic inflammation
• 刊名：Journal of Inflammation
• 出版年：2014
• 出版时间：December 2014
• 年：2014
• 卷：11
• 期：1
• 全文大小：539 KB
• 参考文献：1. Wenzel, RP (2002) Treating sepsis. N Engl J Med 347: pp. 966-967 CrossRef
  2. Dhainaut, JF, Marin, N, Mignon, A, Vinsonneau, C (2001) Hepatic response to sepsis: interaction between coagulation and inflammatory processes. Crit Care Med 29: pp. S42-S47 CrossRef
  3. Matuschak, GM, Rinaldo, JE (1988) Organ interactions in the adult respiratory distress syndrome during sepsis. Role of the liver in host defense. Chest 94: pp. 400-406 CrossRef
  4. Browder, W, Ha, T, Chuanfu, L, Kalbfleisch, JH, Ferguson, DA, Williams, DL (1999) Early activation of pulmonary nuclear factor kappaB and nuclear factor kappaB and nuclear factor interleukin-6 in polymicrobial sepsis. J Trauma 46: pp. 590-596 CrossRef
  5. Yoshidome, H, Kato, A, Edwards, MJ, Lentsch, AB (1999) Interleukin-10 suppresses hepatic ischemia/reperfusion injury in mice: implications of a central role for nuclear factor kappaB. Hepatology 30: pp. 203-208 CrossRef
  6. Gibbs, PE, Maines, MD (2007) Biliverdin inhibits activation of NF-kappaB. reversal of inhibition by human biliverdin reductase. Int J Cancer 121: pp. 2567-2574 CrossRef
  7. Bellezza, I, Tucci, A, Galli, F, Grottelli, S, Mierla, AL, Pilolli, F, Minelli, A (2012) Inhibition of NF-κB nuclear translocation via HO-1 activation underlies α-tocopheryl succinate toxicity. J Nutr Biochem 23: pp. 1583-1591 CrossRef
  8. Mallick, IH, Winslet, MC, Seifalian, AM (2010) Ischemic preconditioning of small bowel mitigates the late phase of reperfusion injury: heme oxygenase mediates cytoprotection. Am J Surg 199: pp. 223-231 CrossRef
  9. Zeynalov, E, Shah, ZA, Li, RC, Dore, S (2009) Heme oxygenase 1 is associated with ischemic preconditioning-induced protection against brain ischemia. Neurobiol Dis 35: pp. 264-269 CrossRef
  10. Xu, B, Gao, X, Xu, J, Lei, S, Xia, ZY, Xu, Y, Xia, Z (2011) Ischemic postconditioning attenuates lung reperfusion injury and reduces systemic proinflammatory cytokine release via heme oxygenase 1. J Surg Res 166: pp. e157-e164 CrossRef
  11. Xia, ZY, Gao, J, Ancharaz, AK, Liu, KX, Xia, Z, Luo, T (2010) Ischaemic post-conditioning protects lung from ischaemia-reperfusion injury by up-regulation of haeme oxygenase-1. Injury 41: pp. 510-516 CrossRef
  12. Lai, IR, Chang, KJ, Chen, CF (2007) The mechanism of hepatic heme oxygenase-1 expression by limb remote ischemic preconditioning. Transplantation 83: pp. 364 CrossRef
  13. Kanoria, S, Seifalian, AM, Williams, R, Davidson, BR (2007) Hind limb remote preconditioning of the liver: a role for nitric oxide and HO-1. Transplantation 83: pp. 363-364 CrossRef
  14. Lai, IR, Chang, KJ, Chen, CF, Tsai, HW (2006) Transient limb ischemia induces remote preconditioning in liver among rats: the protective role of heme oxygenase-1. Transplantation 81: pp. 1311-1317 CrossRef
  15. Tapuria, N, Kumar, Y, Habib, MM, Abu Amara, M, Seifalian, AM, Davidson, BR (2008) Remote ischemic preconditioning: a novel protective method from ischemia reperfusion injury–a review. J Surg Res 150: pp. 304-330 CrossRef
  16. Loukogeorgakis, SP, Williams, R, Panagiotidou, AT, Kolvekar, SK, Donald, A, Cole
• 刊物主题：Molecular Medicine; Immunology; Pharmacology/Toxicology;
• 出版者：BioMed Central
• ISSN：1476-9255

文摘

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--.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--.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--.014). NF-κB activation was significantly attenuated (p--.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--.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.