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 language | English |
|---|---|
| Pages (from-to) | 898-905 |
| Number of pages | 8 |
| Journal | Journal of Anesthesia |
| Volume | 28 |
| Issue number | 6 |
| DOIs | |
| Publication status | Published - 2014 Jan 1 |
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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 journal › Article
}
TY - JOUR
T1 - Remote ischemic preconditioning prevents lipopolysaccharide-induced liver injury through inhibition of NF-κB activation in mice
AU - Shin, Hyeon Ju
AU - Won, Nam Hee
AU - Lee, Hye Won
PY - 2014/1/1
Y1 - 2014/1/1
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.
KW - NF-κB
KW - Remote ischemic preconditioning
KW - Sepsis
KW - TNF-α
UR - http://www.scopus.com/inward/record.url?scp=84918825852&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84918825852&partnerID=8YFLogxK
U2 - 10.1007/s00540-014-1850-6
DO - 10.1007/s00540-014-1850-6
M3 - Article
VL - 28
SP - 898
EP - 905
JO - Journal of Anesthesia
JF - Journal of Anesthesia
SN - 0913-8668
IS - 6
ER -