Role of nuclear factor-κB in volatile anaesthetic preconditioning with sevoflurane during myocardial ischaemia/reperfusion

Chen Wang, Hong Xie, Xia Liu, Qin Qin, Xuemei Wu, Hong Liu, Chunfeng Liu

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

Background and objective Anaesthetic preconditioning (APC) protects against myocardial ischaemia/reperfusion injury. Nuclear factor-κB (NF-κB) has been implicated in APC-induced myocardial protection in vitro. Our study tested the hypothesis that in-vivo APC with sevoflurane is triggered by NF-κB through downregulation of inflammatory mediators and upregulation of antiapoptosis factors to prevent myocardial injury during ischaemia/ reperfusion. Methods In this in-vivo study, rats were anaesthetized and maintained with sodium pentobarbital throughout the experiment. Rats were exposed to 30 min of 2.5% sevoflurane followed by 15 min washout (APC group) or no inhalation anaesthetics (ischaemia/reperfusion group) before ischaemia/ reperfusion. In the sevoflurane group, rats were exposed to 30 min sevoflurane followed by a 165 min washout period. The NF-κB inhibitor parthenolide (PTN) was used before or after exposure to sevoflurane (PTNRAPC group and APCRPTN group). Left ventricular samples were obtained to measure infarct size, pro-inflammation and apoptosis. A P value less than 0.05 was considered significant. Results APC reduced infarct size (34±6%) compared with ischaemia/reperfusion (53±6%, P<0.05). PTN administered before or after APC abolished the cardioprotection (53±5 and 52±7%, respectively, P<0.05). APC decreased the myocardium apoptosis compared with the ischaemia/ reperfusion only group (6±1 vs.19±3%, P<0.05); PTN administered before or after sevoflurane preconditioning abolished this effect. APC induced upregulation of NF-κB p50/p65 before ischaemia (51±4/26±3% vs. 15±1/ 11±1% in the control group, P<0.05). After reperfusion, NF-κB was upregulated in the ischaemia/reperfusion and APC groups, but it was lower in the APC group than in the ischaemia/reperfusion group. PTN administered before and after APC inhibited the expressions. Before ischaemia, Bcl-2 was increased in the APC and sevoflurane groups (94±3 and 102±4%, respectively) compared with the control group (68 ±2%, P<0.05). After reperfusion, intercellular adhesion molecule-1, tumour necrosis factor-a and caspase-3 expressions were significantly increased in the ischaemia/ reperfusion group (92±5, 115±4 and 65±2% compared with the control group, P<0.05); these increases were blunted in the APC group. Conclusion APC with sevoflurane produced myocardial protection against ischaemia/reperfusion in vivo. NF-κB acted not only as a trigger but also as a mediator that played an important role in APC through upregulation of NF-κB and the antiapoptosis protein Bcl-2 during the preconditioning period and then through downregulation of the inflammatory proteins intercellular adhesion molecule-1 and tumour necrosis factor-α during reperfusion, ultimately decreasing caspase-3 expression and apoptosis.

Original languageEnglish (US)
Pages (from-to)747-756
Number of pages10
JournalEuropean Journal of Anaesthesiology
Volume27
Issue number8
DOIs
StatePublished - Aug 2010

Fingerprint

Myocardial Reperfusion
Myocardial Ischemia
Anesthetics
Reperfusion
Ischemia
Up-Regulation
sevoflurane
Intercellular Adhesion Molecule-1
Apoptosis
Reperfusion Injury
Caspase 3
Control Groups
Down-Regulation
Myocardial Ischemic Preconditioning
Tumor Necrosis Factor-alpha
Inhalation Anesthetics
Myocardial Reperfusion Injury
Pentobarbital

Keywords

  • Ischaemia/reperfusion
  • Nuclear factor-κB
  • Preconditioning
  • Sevoflurane

ASJC Scopus subject areas

  • Anesthesiology and Pain Medicine

Cite this

Role of nuclear factor-κB in volatile anaesthetic preconditioning with sevoflurane during myocardial ischaemia/reperfusion. / Wang, Chen; Xie, Hong; Liu, Xia; Qin, Qin; Wu, Xuemei; Liu, Hong; Liu, Chunfeng.

In: European Journal of Anaesthesiology, Vol. 27, No. 8, 08.2010, p. 747-756.

Research output: Contribution to journalArticle

Wang, Chen ; Xie, Hong ; Liu, Xia ; Qin, Qin ; Wu, Xuemei ; Liu, Hong ; Liu, Chunfeng. / Role of nuclear factor-κB in volatile anaesthetic preconditioning with sevoflurane during myocardial ischaemia/reperfusion. In: European Journal of Anaesthesiology. 2010 ; Vol. 27, No. 8. pp. 747-756.
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abstract = "Background and objective Anaesthetic preconditioning (APC) protects against myocardial ischaemia/reperfusion injury. Nuclear factor-κB (NF-κB) has been implicated in APC-induced myocardial protection in vitro. Our study tested the hypothesis that in-vivo APC with sevoflurane is triggered by NF-κB through downregulation of inflammatory mediators and upregulation of antiapoptosis factors to prevent myocardial injury during ischaemia/ reperfusion. Methods In this in-vivo study, rats were anaesthetized and maintained with sodium pentobarbital throughout the experiment. Rats were exposed to 30 min of 2.5{\%} sevoflurane followed by 15 min washout (APC group) or no inhalation anaesthetics (ischaemia/reperfusion group) before ischaemia/ reperfusion. In the sevoflurane group, rats were exposed to 30 min sevoflurane followed by a 165 min washout period. The NF-κB inhibitor parthenolide (PTN) was used before or after exposure to sevoflurane (PTNRAPC group and APCRPTN group). Left ventricular samples were obtained to measure infarct size, pro-inflammation and apoptosis. A P value less than 0.05 was considered significant. Results APC reduced infarct size (34±6{\%}) compared with ischaemia/reperfusion (53±6{\%}, P<0.05). PTN administered before or after APC abolished the cardioprotection (53±5 and 52±7{\%}, respectively, P<0.05). APC decreased the myocardium apoptosis compared with the ischaemia/ reperfusion only group (6±1 vs.19±3{\%}, P<0.05); PTN administered before or after sevoflurane preconditioning abolished this effect. APC induced upregulation of NF-κB p50/p65 before ischaemia (51±4/26±3{\%} vs. 15±1/ 11±1{\%} in the control group, P<0.05). After reperfusion, NF-κB was upregulated in the ischaemia/reperfusion and APC groups, but it was lower in the APC group than in the ischaemia/reperfusion group. PTN administered before and after APC inhibited the expressions. Before ischaemia, Bcl-2 was increased in the APC and sevoflurane groups (94±3 and 102±4{\%}, respectively) compared with the control group (68 ±2{\%}, P<0.05). After reperfusion, intercellular adhesion molecule-1, tumour necrosis factor-a and caspase-3 expressions were significantly increased in the ischaemia/ reperfusion group (92±5, 115±4 and 65±2{\%} compared with the control group, P<0.05); these increases were blunted in the APC group. Conclusion APC with sevoflurane produced myocardial protection against ischaemia/reperfusion in vivo. NF-κB acted not only as a trigger but also as a mediator that played an important role in APC through upregulation of NF-κB and the antiapoptosis protein Bcl-2 during the preconditioning period and then through downregulation of the inflammatory proteins intercellular adhesion molecule-1 and tumour necrosis factor-α during reperfusion, ultimately decreasing caspase-3 expression and apoptosis.",
keywords = "Ischaemia/reperfusion, Nuclear factor-κB, Preconditioning, Sevoflurane",
author = "Chen Wang and Hong Xie and Xia Liu and Qin Qin and Xuemei Wu and Hong Liu and Chunfeng Liu",
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volume = "27",
pages = "747--756",
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TY - JOUR

T1 - Role of nuclear factor-κB in volatile anaesthetic preconditioning with sevoflurane during myocardial ischaemia/reperfusion

AU - Wang, Chen

AU - Xie, Hong

AU - Liu, Xia

AU - Qin, Qin

AU - Wu, Xuemei

AU - Liu, Hong

AU - Liu, Chunfeng

PY - 2010/8

Y1 - 2010/8

N2 - Background and objective Anaesthetic preconditioning (APC) protects against myocardial ischaemia/reperfusion injury. Nuclear factor-κB (NF-κB) has been implicated in APC-induced myocardial protection in vitro. Our study tested the hypothesis that in-vivo APC with sevoflurane is triggered by NF-κB through downregulation of inflammatory mediators and upregulation of antiapoptosis factors to prevent myocardial injury during ischaemia/ reperfusion. Methods In this in-vivo study, rats were anaesthetized and maintained with sodium pentobarbital throughout the experiment. Rats were exposed to 30 min of 2.5% sevoflurane followed by 15 min washout (APC group) or no inhalation anaesthetics (ischaemia/reperfusion group) before ischaemia/ reperfusion. In the sevoflurane group, rats were exposed to 30 min sevoflurane followed by a 165 min washout period. The NF-κB inhibitor parthenolide (PTN) was used before or after exposure to sevoflurane (PTNRAPC group and APCRPTN group). Left ventricular samples were obtained to measure infarct size, pro-inflammation and apoptosis. A P value less than 0.05 was considered significant. Results APC reduced infarct size (34±6%) compared with ischaemia/reperfusion (53±6%, P<0.05). PTN administered before or after APC abolished the cardioprotection (53±5 and 52±7%, respectively, P<0.05). APC decreased the myocardium apoptosis compared with the ischaemia/ reperfusion only group (6±1 vs.19±3%, P<0.05); PTN administered before or after sevoflurane preconditioning abolished this effect. APC induced upregulation of NF-κB p50/p65 before ischaemia (51±4/26±3% vs. 15±1/ 11±1% in the control group, P<0.05). After reperfusion, NF-κB was upregulated in the ischaemia/reperfusion and APC groups, but it was lower in the APC group than in the ischaemia/reperfusion group. PTN administered before and after APC inhibited the expressions. Before ischaemia, Bcl-2 was increased in the APC and sevoflurane groups (94±3 and 102±4%, respectively) compared with the control group (68 ±2%, P<0.05). After reperfusion, intercellular adhesion molecule-1, tumour necrosis factor-a and caspase-3 expressions were significantly increased in the ischaemia/ reperfusion group (92±5, 115±4 and 65±2% compared with the control group, P<0.05); these increases were blunted in the APC group. Conclusion APC with sevoflurane produced myocardial protection against ischaemia/reperfusion in vivo. NF-κB acted not only as a trigger but also as a mediator that played an important role in APC through upregulation of NF-κB and the antiapoptosis protein Bcl-2 during the preconditioning period and then through downregulation of the inflammatory proteins intercellular adhesion molecule-1 and tumour necrosis factor-α during reperfusion, ultimately decreasing caspase-3 expression and apoptosis.

AB - Background and objective Anaesthetic preconditioning (APC) protects against myocardial ischaemia/reperfusion injury. Nuclear factor-κB (NF-κB) has been implicated in APC-induced myocardial protection in vitro. Our study tested the hypothesis that in-vivo APC with sevoflurane is triggered by NF-κB through downregulation of inflammatory mediators and upregulation of antiapoptosis factors to prevent myocardial injury during ischaemia/ reperfusion. Methods In this in-vivo study, rats were anaesthetized and maintained with sodium pentobarbital throughout the experiment. Rats were exposed to 30 min of 2.5% sevoflurane followed by 15 min washout (APC group) or no inhalation anaesthetics (ischaemia/reperfusion group) before ischaemia/ reperfusion. In the sevoflurane group, rats were exposed to 30 min sevoflurane followed by a 165 min washout period. The NF-κB inhibitor parthenolide (PTN) was used before or after exposure to sevoflurane (PTNRAPC group and APCRPTN group). Left ventricular samples were obtained to measure infarct size, pro-inflammation and apoptosis. A P value less than 0.05 was considered significant. Results APC reduced infarct size (34±6%) compared with ischaemia/reperfusion (53±6%, P<0.05). PTN administered before or after APC abolished the cardioprotection (53±5 and 52±7%, respectively, P<0.05). APC decreased the myocardium apoptosis compared with the ischaemia/ reperfusion only group (6±1 vs.19±3%, P<0.05); PTN administered before or after sevoflurane preconditioning abolished this effect. APC induced upregulation of NF-κB p50/p65 before ischaemia (51±4/26±3% vs. 15±1/ 11±1% in the control group, P<0.05). After reperfusion, NF-κB was upregulated in the ischaemia/reperfusion and APC groups, but it was lower in the APC group than in the ischaemia/reperfusion group. PTN administered before and after APC inhibited the expressions. Before ischaemia, Bcl-2 was increased in the APC and sevoflurane groups (94±3 and 102±4%, respectively) compared with the control group (68 ±2%, P<0.05). After reperfusion, intercellular adhesion molecule-1, tumour necrosis factor-a and caspase-3 expressions were significantly increased in the ischaemia/ reperfusion group (92±5, 115±4 and 65±2% compared with the control group, P<0.05); these increases were blunted in the APC group. Conclusion APC with sevoflurane produced myocardial protection against ischaemia/reperfusion in vivo. NF-κB acted not only as a trigger but also as a mediator that played an important role in APC through upregulation of NF-κB and the antiapoptosis protein Bcl-2 during the preconditioning period and then through downregulation of the inflammatory proteins intercellular adhesion molecule-1 and tumour necrosis factor-α during reperfusion, ultimately decreasing caspase-3 expression and apoptosis.

KW - Ischaemia/reperfusion

KW - Nuclear factor-κB

KW - Preconditioning

KW - Sevoflurane

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