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

doi:10.1007/s00540-014-1850-6

Cited by 17 publications

(14 citation statements)

References 27 publications

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“…It is reported that sevoflurane can alleviate oxidative stress in I/R organ [32], which may attenuate I/R injury. Alternatively, anti-inflammatory properties of RIPC may be associated with the inhibition of the NF-κB by suppressing its nuclear translocation [33]. Moreover, less secretion of inflammatory cytokines was observed in SPC combined RIPC group compared with those in SPC or RIPC groups.…”

Section: Discussionmentioning

confidence: 95%

Remote Ischaemic Preconditioning and Sevoflurane Postconditioning Synergistically Protect Rats from Myocardial Injury Induced by Ischemia and Reperfusion Partly via Inhibition TLR4/MyD88/NF-κB Signaling Pathway

Zhang

et al. 2017

Cell Physiol Biochem

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Background/Aims: A combination sevoflurane postconditioning (SPC) and remote ischemic preconditioning (RIPC) is proved effective in an ex vivo rat heart perfusion model. However, the combined effect of those two interventions is not tested in rat myocardial ischemia/reperfusion (I/R) model, and the underlying mechanisms remain to be elucidated. This study aimed to investigate the effect in vivo using a rat myocardial I/R model and illuminate the related mechanisms. Methods: Forty male Sprague-Dawley rats were randomly divided into the following 5 groups: i) sham-operated control; ii) I/R; iii) I/R + RIPC; iv) I/R + SPC; v) I/R + RIPC + SPC. The hemodynamic parameters were recorded at the end of reperfusion. The histological changes including the infarct size were assessed using Triphenyltetrazolium chloride (TTC) staining and H&E staining. In addition, the circulating levels of cardiac enzymes (CK-MB, hs-cTnT, and cTnT) inflammatory cytokines (IL-6, IL-8, and TNF-α) were detected. The expression levels of apoptosis-related proteins (C-Caspase 3, PARP, Bax, and Bcl-2), proinflammatory factors (TLR4, HMGB-1, MyD88, and p65), and IKB-α were measured by Western blot analysis. Real-time PCR was performed to detect mRNA levels of the proinflammatory factors. Results: Both SPC and RIPC significantly reduced the infarct size, cardiac enzyme release, inflammatory cytokine secretion, and proinflammatory factor expression, and increased IKB-α expression compared to I/R group. Furthermore, the combination of those two strategies had synergic infarct size limiting and anti-inflammatory effects. Conclusions: The finding of this study suggested that the combination of SPC and RIPC had a potentially cardioprotective effect through inhibiting TLR4/MyD88/NF-κB signaling.

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Section: Discussionmentioning

confidence: 95%

Remote Ischaemic Preconditioning and Sevoflurane Postconditioning Synergistically Protect Rats from Myocardial Injury Induced by Ischemia and Reperfusion Partly via Inhibition TLR4/MyD88/NF-κB Signaling Pathway

Zhang

et al. 2017

Cell Physiol Biochem

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“…Reperfusion was accomplished by cutting the elastic rings with scissors, confirmed by the disappearance of blue color to the limbs (Figure A1) as described previously [86,87,88]. The mice were anesthetized with isoflurane in O 2 /N 2 O (5% isoflurane for induction and 2%–3% to maintain anesthesia) during RIPC treatment and treatment consisted of three cycles of 4-min ischemia interspersed with 4-min reperfusion.…”

Section: Methodsmentioning

confidence: 99%

Effects of Remote Ischemic Preconditioning on Heme Oxygenase-1 Expression and Cutaneous Wound Repair

Cremers

Wever

Wong

et al. 2017

IJMS

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Skin wounds may lead to scar formation and impaired functionality. Remote ischemic preconditioning (RIPC) can induce the anti-inflammatory enzyme heme oxygenase-1 (HO-1) and protect against tissue injury. We aim to improve cutaneous wound repair by RIPC treatment via induction of HO-1. RIPC was applied to HO-1-luc transgenic mice and HO-1 promoter activity and mRNA expression in skin and several other organs were determined in real-time. In parallel, RIPC was applied directly or 24h prior to excisional wounding in mice to investigate the early and late protective effects of RIPC on cutaneous wound repair, respectively. HO-1 promoter activity was significantly induced on the dorsal side and locally in the kidneys following RIPC treatment. Next, we investigated the origin of this RIPC-induced HO-1 promoter activity and demonstrated increased mRNA in the ligated muscle, heart and kidneys, but not in the skin. RIPC did not change HO-1 mRNA and protein levels in the wound 7 days after cutaneous injury. Both early and late RIPC did not accelerate wound closure nor affect collagen deposition. RIPC induces HO-1 expression in several organs, but not the skin, and did not improve excisional wound repair, suggesting that the skin is insensitive to RIPC-mediated protection.

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“…Mice were randomly assigned to be either controls or to undergo remote IPC in which blood flow to a hind limb was occluded with a rubber band three times for ten minutes each time and separated by a ten minute period of reperfusion. Remote IPC was found to inhibit NF-κB activity with concomitant attenuation of TNF-α expression, neutrophil accumulation, and microabscess formation in the liver, thus protecting the liver from subsequent IR insult (Shin et al, 2014[69]). Finally, IPC was shown to attenuate expression of TNF-α and ICAM-1 in hepatocytes using a murine model of IR.…”

Section: Ipc Inhibits Expression Of Nf-κb and Proinflammatory Cytokinmentioning

confidence: 99%

Ischemic preconditioning modulates ROS to confer protection in liver ischemia and reperfusion

Bystrom

Foley

Toledo‐Pereyra

et al. 2017

EXCLI Journal; 16:Doc483; ISSN 1611-2156

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

Abstract: 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.

Cited by 17 publications

References 27 publications

Remote Ischaemic Preconditioning and Sevoflurane Postconditioning Synergistically Protect Rats from Myocardial Injury Induced by Ischemia and Reperfusion Partly via Inhibition TLR4/MyD88/NF-κB Signaling Pathway

Remote Ischaemic Preconditioning and Sevoflurane Postconditioning Synergistically Protect Rats from Myocardial Injury Induced by Ischemia and Reperfusion Partly via Inhibition TLR4/MyD88/NF-κB Signaling Pathway

Effects of Remote Ischemic Preconditioning on Heme Oxygenase-1 Expression and Cutaneous Wound Repair

Ischemic preconditioning modulates ROS to confer protection in liver ischemia and reperfusion

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