Remote ischemic preconditioning prevents lipopolysaccharide-induced liver injury through inhibition of NF-κB activation in mice

Hyeon Ju Shin, Nam Hee Won, Hye Won Lee

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

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.

Purpose: 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.

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.

Conclusion: 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.

Original languageEnglish
Pages (from-to)898-905
Number of pages8
JournalJournal of Anesthesia
Volume28
Issue number6
DOIs
Publication statusPublished - 2014 Jan 1

Fingerprint

Ischemic Preconditioning
Lipopolysaccharides
Liver
Wounds and Injuries
Tumor Necrosis Factor-alpha
Injections
Sepsis
Ischemia
Extremities
Tourniquets
Neutrophil Activation
Rubber
Endotoxins
Reperfusion
Neutrophils
Control Groups

Keywords

  • NF-κB
  • Remote ischemic preconditioning
  • Sepsis
  • TNF-α

ASJC Scopus subject areas

  • Anesthesiology and Pain Medicine

Cite this

Remote ischemic preconditioning prevents lipopolysaccharide-induced liver injury through inhibition of NF-κB activation in mice. / Shin, Hyeon Ju; Won, Nam Hee; Lee, Hye Won.

In: Journal of Anesthesia, Vol. 28, No. 6, 01.01.2014, p. 898-905.

Research output: Contribution to journalArticle

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N2 - 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.Purpose: 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.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.Conclusion: 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.

AB - 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.Purpose: 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.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.Conclusion: 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.

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