Propofol post-conditioning protects against cardiomyocyte apoptosis in hypoxia/reoxygenation injury by suppressing nuclear factor-kappa B translocation via extracellular signal-regulated kinase mitogen-activated protein kinase pathway

Li, Hao; Tan, Jian; Zou, Zui; Huang, Chun; Xue-yin, Shi

doi:10.1097/eja.0b013e32834296d5

Cited by 21 publications

(29 citation statements)

References 31 publications

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“…Prepared propofol was added to the medium at different concentrations of 0, 25, 50 or 100 µM for 30 min prior to IHR exposure, and kept in the medium throughout the entire experiment. This dose range for propofol was selected from a previous study and considered as the range of concentrations that was clinically relevant (15). Cells that were not treated with either propofol or IHR were used as a control.…”

Section: Methodsmentioning

confidence: 99%

“…An in vitro study has demonstrated that propofol post-conditioning inhibits the activation of NF-κB induced by hypoxia/reoxygenation and protects cardiomyocytes against apoptosis (15). Other studies reported that propofol suppresses the activation of HIF-1 induced by lipopolysaccharides or hypoxia in macrophages (24), alveolar epithelial cells (25) and lung epithelial cells (22).…”

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confidence: 99%

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Propofol selectively inhibits nuclear factor-κB activity by suppressing p38 mitogen-activated protein kinase signaling in human EA.hy926 endothelial cells during intermittent hypoxia/reoxygenation

Zhang

2014

Molecular Medicine Reports

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Abstract. Intermittent hypoxia/reoxygenation (IHR) induces proinflammatory cytokines, contributing to the pathogenic process of atherosclerosis associated with obstructive sleep apnea (OSA). Two transcription factors, nuclear factor-κB (NF-κB) and hypoxia-inducible factor-1 (HIF-1), have been indicated to mediate proinflammatory cytokines during IHR. The anti-inflammatory effects of propofol have attracted increasing attention in regard to the treament of multiple diseases associated with inflammation. The present study examined whether propofol inhibits NF-κB and HIF-1 activity in vascular endothelial cells during IHR. EA.hy926 endothelial cells were exposed to IHR for 64 cycles with or without propofol treatment. Gene knockdown by transfection of siRNA against p38 mitogen-activated protein kinase (MAPK) was also used to investigate the molecular mechanisms. Compared with the control group, IHR exposure significantly induced the activation of NF-κB and HIF-1, enhanced the mRNA expression of proinflammatory cytokines and increased the activation of p38 MAPK. Propofol dose-dependently inhibited the IHR-induced activation of NF-κB, but did not change the activation of HIF-1, which was accompanied by decreased levels of proinflammatory cytokines. In addition, IHR-induced p38 MAPK activity was attenuated by propofol in a similar manner to the reduction in NF-κB activity. Furthermore, knockdown of p38 MAPK with siRNA significantly reduced the IHR-induced activation of NF-κB, while not affecting HIF-1. These data demonstrate that propofol selectively attenuates the IHR-induced activation of NF-κB, but not HIF-1, in vascular endothelial cells, and these beneficial effects are likely to be based on the inhibition of the p38 MAPK signaling pathway. Propofol may have the potential to prevent atherosclerosis in patients with OSA by inhibiting NF-κB-mediated inflammation in the vascular endothelium.

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Section: Methodsmentioning

confidence: 99%

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confidence: 99%

Propofol selectively inhibits nuclear factor-κB activity by suppressing p38 mitogen-activated protein kinase signaling in human EA.hy926 endothelial cells during intermittent hypoxia/reoxygenation

Zhang

2014

Molecular Medicine Reports

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“…The potential molecular mechanisms include antioxidation, anti-inflammation, or activating cardioprotective signaling pathways [10–12]. However, little is known about the direct upstreaming target or initiating molecule.…”

Section: Introductionmentioning

confidence: 99%

Activation of Endocannabinoid Receptor 2 as a Mechanism of Propofol Pretreatment‐Induced Cardioprotection against Ischemia‐Reperfusion Injury in Rats

Sun

Lü

Wang

et al. 2017

Oxidative Medicine and Cellular Longevity

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Propofol pretreatment before reperfusion, or propofol conditioning, has been shown to be cardioprotective, while its mechanism is unclear. The current study investigated the roles of endocannabinoid signaling in propofol cardioprotection in an in vivo model of myocardial ischemia/reperfusion (I/R) injury and in in vitro primary cardiomyocyte hypoxia/reoxygenation (H/R) injury. The results showed that propofol conditioning increased both serum and cell culture media concentrations of endocannabinoids including anandamide (AEA) and 2-arachidonoylglycerol (2-AG) detected by LC-MS/MS. The reductions of myocardial infarct size in vivo and cardiomyocyte apoptosis and death in vitro were accompanied with attenuations of oxidative injuries manifested as decreased reactive oxygen species (ROS), malonaldehyde (MDA), and MPO (myeloperoxidase) and increased superoxide dismutase (SOD) production. These effects were mimicked by either URB597, a selective endocannabinoids degradation inhibitor, or VDM11, a selective endocannabinoids reuptake inhibitor. In vivo study further validated that the cardioprotective and antioxidative effects of propofol were reversed by selective CB2 receptor antagonist AM630 but not CB1 receptor antagonist AM251. We concluded that enhancing endogenous endocannabinoid release and subsequent activation of CB2 receptor signaling represent a major mechanism whereby propofol conditioning confers antioxidative and cardioprotective effects against myocardial I/R injury.

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“…As a result, insulin resistance is generated or aggravated (29,32,33). Previous studies have demonstrated that propofol inhibits NF-κB activity in various tissues or cells (34)(35)(36)(37)(38). Therefore, it was hypothesized that the protective effect of propofol against TNF-α-induced insulin resistance in primary mouse hepatocytes may be associated with the inhibitory effect of propofol on the NF-κB signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

Protective effect of pretreatment with propofol against tumor necrosis factor-α-induced hepatic insulin resistance

Zhou

Wang

Yang

et al. 2015

Experimental and Therapeutic Medicine

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Propofol post-conditioning protects against cardiomyocyte apoptosis in hypoxia/reoxygenation injury by suppressing nuclear factor-kappa B translocation via extracellular signal-regulated kinase mitogen-activated protein kinase pathway

Abstract: Propofol exerts cardioprotection when administered at the early phase of reperfusion. The effect is mediated through decrease in cardiomyocyte apoptosis and NF-κB nucleus translocation potentially via ERK signalling pathways.

Cited by 21 publications

References 31 publications

Propofol selectively inhibits nuclear factor-κB activity by suppressing p38 mitogen-activated protein kinase signaling in human EA.hy926 endothelial cells during intermittent hypoxia/reoxygenation

Propofol selectively inhibits nuclear factor-κB activity by suppressing p38 mitogen-activated protein kinase signaling in human EA.hy926 endothelial cells during intermittent hypoxia/reoxygenation

Activation of Endocannabinoid Receptor 2 as a Mechanism of Propofol Pretreatment‐Induced Cardioprotection against Ischemia‐Reperfusion Injury in Rats

Protective effect of pretreatment with propofol against tumor necrosis factor-α-induced hepatic insulin resistance

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