Postconditioning in Reperfusion Injury: A Status Report

Zhao, Zhi‐Qing

doi:10.1007/s10557-010-6240-1

Cited by 63 publications

(46 citation statements)

References 122 publications

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“…Patients suffering from these diseases are often at increased risk of myocardial I/R injury, which is an important reason for increasing perioperative complications and mortality [3] . A series of brief episodes of ischemia and reperfusion at the onset of reperfusion can reduce myocardial infarct size, known as "ischemic post-conditioning" [4,5] . However, it is difficult to apply ischemic post-conditioning to clinical practice because well-controlled, short episodes of myocardial ischemia are almost impossible to perform.…”

Section: Introductionmentioning

confidence: 99%

Sevoflurane post-conditioning protects isolated rat hearts against ischemia-reperfusion injury via activation of the ERK1/2 pathway

et al. 2014

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Aim: To investigate the role of extracellular signal-regulated kinases (ERKs) in sevoflurane post-conditioning induced cardioprotection in vitro. Methods: Isolated rat hearts were subjected to 30 min ischemia followed by 120 min reperfusion (I/R). Sevoflurane post-conditioning was carried out by administration of O 2 -enriched gas mixture with 3% sevoflurane (SEVO) for 15 min from the onset of reperfusion. Cardiac functions, myocardial infarct size, myocardial ATP and NAD + contents, mitochondrial ultrastructure, and anti-apototic and antioncosis protein levels were measured. Results: Sevoflurane post-conditioning significantly improved the heart function, decreased infarct size and mitochondria damage, and increased myocardial ATP and NAD + content in the I/R hearts. Furthermore, sevoflurane post-conditioning significantly increased the levels of p-ERK and p-p70S6K, decreased the levels of porimin, caspase-8, cleaved caspase-3, and cytosolic cytochrome c in the I/R hearts. Co-administration of the ERK1/2 inhibitor PD98059 (20 μmol/L) abolished the sevoflurane-induced protective effects against myocardial I/R. Conclusion: Sevoflurane post-conditioning protects isolated rat hearts against myocardial I/R injury and inhibits cell oncosis and apoptosis via activation of the ERK1/2 pathway.

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Section: Introductionmentioning

confidence: 99%

Sevoflurane post-conditioning protects isolated rat hearts against ischemia-reperfusion injury via activation of the ERK1/2 pathway

et al. 2014

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“…One of the promising approaches for reducing cardiac ischemia-reperfusion injury is ischemic postconditioning, a phenomenon of infarct size reduction caused by induction of repetitive brief episodes of ischemia during early reperfusion after a prolonged ischemic insult. 3,4 In recent years, it has been shown both in the experimental and clinical settings that the infarct-limiting effect of ischemic postconditioning can be mimicked by administration of certain cardioprotective drugs at the time of myocardial reperfusion or just prior to it. 5 This phenomenon has been termed "pharmacological postconditioning".…”

Section: Introductionmentioning

confidence: 99%

Passive targeting of ischemic-reperfused myocardium with adenosine-loaded silica nanoparticles

Galagudza¹,

Королев²,

Постнов³

et al. 2012

IJN

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Pharmacological agents suggested for infarct size limitation have serious side effects when used at cardioprotective doses which hinders their translation into clinical practice. The solution to the problem might be direct delivery of cardioprotective drugs into ischemic-reperfused myocardium. In this study, we explored the potential of silica nanoparticles for passive delivery of adenosine, a prototype cardioprotective agent, into ischemic-reperfused heart tissue. In addition, the biodegradation of silica nanoparticles was studied both in vitro and in vivo. Immobilization of adenosine on the surface of silica nanoparticles resulted in enhancement of adenosine-mediated infarct size limitation in the rat model. Furthermore, the hypotensive effect of adenosine was attenuated after its adsorption on silica nanoparticles. We conclude that silica nanoparticles are biocompatible materials that might potentially be used as carriers for heart-targeted drug delivery.

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“…4 Despite numerous attempts to improve the outcome in patients with ARDS, a mortality rate around 50% is still encountered. 5 Ischemic post-conditioning (IPo) has been demonstrated to be beneficial following ischemia/reperfusion (IR) injury in the heart, brain, liver, kidney, and spinal cord, 6 and its mechanical interventions against reperfusion injury relate to multiple and interacting components in endogenous protective mechanisms. Previous studies have shown that IPo can also attenuate lung injury induced by IIR, in part, through the activation of heme oxygenase-1 (HO-1).…”

mentioning

confidence: 99%

Ischemic post-conditioning attenuates acute lung injury induced by intestinal ischemia–reperfusion in mice: role of Nrf2

Meng

Cao²,

et al. 2016

Laboratory Investigation

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Intestinal ischemic post-conditioning (IPo) protects against lung injury induced by intestinal ischemia-reperfusion (IIR) partly through promotion of expression and function of heme oxygenase-1 (HO-1). NF-E2-related factor-2 (Nrf2) is a key transcription factor that interacts with HO-1 and regulates antioxidant defense. However, the role of Nrf2 in IPo protection of IIR-induced pulmonary injury is not completely understood. Here we show that IPo significantly attenuated IIR-induced lung injury and suppressed oxidative stress and systemic inflammatory responses. IPo also increased the expression of both Nrf2 and HO-1. Consistently, the beneficial effects of IPo were abolished by ATRA and Brusatol, potent inhibitors of Nrf2. Moreover, the Nrf2 agonist t-BHQ showed similar activity as IPo. Taken together, our data suggest that Nrf2 activity, along with HO-1, plays an important role in the protective effects of IPo against IIR-induced acute lung injury.

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Postconditioning in Reperfusion Injury: A Status Report

Cited by 63 publications

References 122 publications

Sevoflurane post-conditioning protects isolated rat hearts against ischemia-reperfusion injury via activation of the ERK1/2 pathway

Sevoflurane post-conditioning protects isolated rat hearts against ischemia-reperfusion injury via activation of the ERK1/2 pathway

Passive targeting of ischemic-reperfused myocardium with adenosine-loaded silica nanoparticles

Ischemic post-conditioning attenuates acute lung injury induced by intestinal ischemia–reperfusion in mice: role of Nrf2

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