Ischemic preconditioning: a defense mechanism against the reactive oxygen species generated after hepatic ischemia reperfusion1

Peralta, Carmen; Bulbena, O.; Xaus, Carme; Prats, Neus; Cutrìn, Juan Carlos; Poli, Giuseppe; Gelpí, Emili; Roselló‐Catafau, Joan

doi:10.1097/00007890-200204270-00004

Cited by 95 publications

(92 citation statements)

References 43 publications

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“…The results are in agreement with the reports of Cavalieri et al [5] . Peralta et al [6] , showed that IPC could block the xanthine oxidase pathway of ROS generation, thus providing protection against liver I/R injury. Diminishing ROS production contributes to the mechanism of IPC injury-preventive effects.…”

Section: Discussionmentioning

confidence: 99%

“…Administration of antioxidants such as glutathione, quercetin, could afford protection against ischemia/ reperfusion injury [3,4] . It has been shown that ischemic preconditioning can prevent the formation of ROS after I/ R, thus exerting protection to the liver [5,6] . To control the detrimental effects of ROS, organisms have developed a variety of antioxidant defense systems, especially the endogenous antioxidant enzymes system including superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx).…”

Section: Introductionmentioning

confidence: 99%

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Modulation of liver oxidant-antioxidant system by ischemic preconditioning during ischemia/reperfusion injury in rats

Yuan

Ma²,

Gong³

et al. 2005

WJG

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AIM:To investigate effects of ischemic pre-conditioning on the liver endogenous oxidant-antioxidant system during ischemia/reperfusion injury. METHODS:Twenty-four male Sprague-Dawley rats were randomly divided into sham-operated (Sham), ischemia/ reperfusion (I/R), ischemic pre-conditioning plus ischemia/ reperfusion (IPC) groups. Serum ALT, AST and hyaluronic acid levels were assayed and pathologic alterations observed. Liver malondialdehyde (MDA) contents, endogenous antioxidant enzymes, superoxidase dismutase (SOD), catalase (CAT), gultathionine peroxidase (GSH-Px) activities, neutrophils accumulation marker, myeloperoxidase (MPO) activities were measured respectively. RESULTS:Compared with I/R group, sinusoidal endothelial cells as well as hepatocytes damages, as assessed biochemically and histochemically, were improved significantly in IPC group; neutrophils infiltration was also markedly reduced. In IPC group, liver peroxidation, as measured by MDA contents, was significantly decreased when compared with I/R group; endogenous antioxidant enzymes, SOD, CAT and GSH-Px activities were markedly higher than that in I/R group. CONCLUSION:Ischemic pre-conditioning exerts protective effects on both hepatic sinusoidal endothelial cells and hepatocytes during liver I/R injury. Its mechanisms may involve dimunition of neutrophils infiltration and modulation of the imbalance of endogenous oxidant-antioxidant system in the organism.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Modulation of liver oxidant-antioxidant system by ischemic preconditioning during ischemia/reperfusion injury in rats

Yuan

Ma²,

Gong³

et al. 2005

WJG

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“…Because administration of antibodies against Pselectin or TNF-␣ prior to ischemia was seen to have the same effect as preconditioning, it has been suggested that the blockade of P-selectin upregulation probably results from inhibition of systemic TNF release from Kupffer cells [88]. Moreover, recently it was reported that ischemic preconditioning was able to increase the hepatic tolerance against reperfusion injury by attenuating the release of ET [89] and the production of ROS, either by blocking the xanthine-oxidase pathway or by preserving the mitochondria structure [90,91]. In this last work it was also reported that well-preserved mitochondria were associated with an attenuated release of cytochrome c to the cytoplasm, as well as with a low index of caspase-3 activity [91].…”

Section: Protective Mechanisms Of Delayed Ischemic Preconditioningmentioning

confidence: 97%

Microvascular dysfunction induced by reperfusion injury and protective effect of ischemic preconditioning

Cutrn

Perrelli

Cavalieri

et al. 2002

Free Radical Biology and Medicine

150

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Abstract-Hepatic ischemia/reperfusion injury has immediate and deleterious effects on the outcome of patients after liver surgery. The precise mechanisms leading to the damage have not been completely elucidated. However, there is substantial evidence that the generation of oxygen free radicals and disturbances of the hepatic microcirculation are involved in this clinical syndrome. Microcirculatory dysfunction of the liver seems to be mediated by sinusoidal endothelial cell damage and by the imbalance of vasoconstrictor and vasodilator molecules, such as endothelin (ET), reactive oxygen species (ROS), and nitric oxide (NO). This may lead to no-reflow phenomenon with release of proinflammatory cytokines, sinusoidal plugging of neutrophils, oxidative stress, and as an ultimate consequence, hypoxic cell injury and parenchymal failure. An inducible potent endogenous mechanism against ischemia/reperfusion injury has been termed ischemic preconditioning. It has been suggested that preconditioning could inhibit the effects of different mediators involved in the microcirculatory dysfunction, including endothelin, tumor necrosis factor-␣, and oxygen free radicals. In this review, we address the mechanisms of liver microcirculatory dysfunction and how ischemic preconditioning could help to provide new surgical and/or pharmacological strategies to protect the liver against reperfusion damage.

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“…The underlying mechanism is thought to rely on the modification of gene expression resulting in protein production as its effectors [110] . Various substances have been implicated as key effectors in liver IPC including adenosine [111][112][113][114] , protein kinase C [115][116][117] , NO [118][119][120][121] , heatshock proteins [122,123] , tyrosine kinases [124] , MAPKs [117] , oxidative stress [125,126] and NF-κB [127,128] . The beneficial effects of IPC on the liver following IRI include decrease in severity of liver necrosis [129] , antiapoptotic effects [130] , preservation of liver microcirculation [131,132] and improvement in survival rate [119] , and more recently, its role in liver regeneration is currently being evaluated.…”

Section: Ischaemic Preconditioning In Liver Regenerationmentioning

confidence: 99%

Role of ischaemic preconditioning in liver regeneration following major liver resection and transplantation

Gomez¹

2007

WJG

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Liver ischaemic preconditioning (IPC) is known to protect the liver from the detrimental effects of ischaemicreperfusion injury (IRI), which contributes significantly to the morbidity and mortality following major liver surgery. Recent studies have focused on the role of IPC in liver regeneration, the precise mechanism of which are not completely understood. This review discusses the current understanding of the mechanism of liver regeneration and the role of IPC in this setting. Relevant articles were reviewed from the published literature using the Medline database. The search was performed using the keywords "liver", "ischaemic reperfusion", "ischaemic preconditioning", "regeneration", "hepatectomy" and "transplantation". The underlying mechanism of liver regeneration is a complex process involving the interaction of cytokines, growth factors and the metabolic demand of the liver. IPC, through various mediators, promotes liver regeneration by up-regulating growthpromoting factors and suppresses growth-inhibiting factors as well as damaging stresses. The increased understanding of the cellular mechanisms involved in IPC will enable the development of alternative treatment modalities aimed at promoting liver regeneration following major liver resection and transplantation.

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Ischemic preconditioning: a defense mechanism against the reactive oxygen species generated after hepatic ischemia reperfusion1

Abstract: Preconditioning, by blocking the xanthine/XOD pathway for ROS generation, would confer protection against the liver and lung injuries induced by hepatic I/R.

Cited by 95 publications

References 43 publications

Modulation of liver oxidant-antioxidant system by ischemic preconditioning during ischemia/reperfusion injury in rats

Modulation of liver oxidant-antioxidant system by ischemic preconditioning during ischemia/reperfusion injury in rats

Microvascular dysfunction induced by reperfusion injury and protective effect of ischemic preconditioning

Role of ischaemic preconditioning in liver regeneration following major liver resection and transplantation

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