Hyperbaric Oxygen Preconditioning Attenuates Myocardium Ischemia-Reperfusion Injury Through Upregulation of Heme Oxygenase 1 Expression

Yin, Xiaoli; Wang, Xiaofeng; Fan, Zhipeng; Peng, Chenghai; Ren, Zhongqiao; Huang, Le; Liu, Zhuang; Zhao, Kun

doi:10.1177/1074248414568196

Cited by 41 publications

(25 citation statements)

References 54 publications

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“…20,41,42 In our study, we investigated the effects of Nar on the Nrf2 translocation and phosphorylation of AKT, PKCδ, and ERK1/2 at different time points. 20,41,42 In our study, we investigated the effects of Nar on the Nrf2 translocation and phosphorylation of AKT, PKCδ, and ERK1/2 at different time points.…”

Section: Discussionmentioning

confidence: 99%

Naringin protects against anoxia/reoxygenation-induced apoptosis in H9c2 cells via the Nrf2 signaling pathway

et al. 2015

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Naringin (Nar) is a major and active flavanone glycoside derivative of several citrus species. The antioxidant properties of Nar have an important function in its cardioprotective effects in various models. However, the effects of Nar on Nrf2 activation and the expression of its downstream genes in myocardial cells are yet to be elucidated. This study was designed to investigate the protective effects of Nar against anoxia/reoxygenation (A/R)-induced injury in H9c2 cells and determine its effects on the activity of Nrf2 and the expression of phase II antioxidant enzymes. H9c2 cells were pretreated with Nar for 6 h before exposure to A/R. A/R treatment severely injured the H9c2 cells, which was accompanied by apoptosis. Nar also suppressed the A/R-induced mitochondrial membrane depolarization and caspase-3 activation. Nar pretreatment significantly reduced the apoptotic rate by enhancing the endogenous anti-oxidative activity of superoxide dismutase, glutathione peroxidase, and catalase, thereby inhibiting intracellular reactive oxygen species generation. Moreover, the presence of Nar alone in H9c2 cells increased the nuclear translocation of Nrf2 in a dose- and time-dependent manner, as well as consistently increased the protein levels of heme oxygenase (HO-1) and glutamate cysteine ligase (GCLC). Nar increased the phosphorylation of ERK1/2, PKCδ, and AKT. However, the Nar-mediated Nrf2 activation and cardioprotection were abolished through the genetic silencing of Nrf2 by siRNA and partially inhibited by specific inhibitors of ERK1/2, PKCδ, and AKT. Therefore, Nar provided cardioprotection by inducing the phosphorylation of ERK1/2, PKCδ, and AKT, which subsequently activated Nrf2 and its downstream genes.

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Section: Discussionmentioning

confidence: 99%

Naringin protects against anoxia/reoxygenation-induced apoptosis in H9c2 cells via the Nrf2 signaling pathway

et al. 2015

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“…In addition, HBO therapy may attenuate hypoxia in marginally perfused tissue (sometimes referred to as the "ischemic penumbra"), and this may be useful in avoiding cell death and restoring function [17]. Recent research suggests that HBO prevents myocardium from ischemia injury by suppression of apoptotic pathways (blockage of caspase-3 activity and protection against Bax/Bcl-2-mediated apoptosis) [18] and protects MIRI via PI3K/Akt/ Nrf2-dependent antioxidant defensive system in animal models [19]. Moreover, for people with acute coronary syndrome, there is some evidence from clinical trial to suggest that HBO is associated with a reduction in the risk of death, the volume of damaged muscle and the risk of major adverse cardiac events [20].…”

Section: Introductionmentioning

confidence: 99%

Cardioprotective Effects of Combined Therapy with Hyperbaric Oxygen and Diltiazem Pretreatment on Myocardial Ischemia-Reperfusion Injury in Rats

Chen

Nong³

et al. 2016

Cell Physiol Biochem

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Background/Aims: In this study, we examined whether the combination of hyperbaric oxygen (HBO) and diltiazem therapy provided a cardioprotective effect on myocardial ischemia-reperfusion injury (MIRI) rat model. Methods: Sixty healthy Sprague-Dawley rats were randomly divided into sham, IR, diltiazem (5 mg/kg), HBO (0.25 MPa, 60 min) and combination therapy (HBO plus diltiazem) groups. MIRI model was established by ligating the left anterior descending for 30 min, followed by 60 min of reperfusion. Results: The results show that HBO and diltiazem preconditioning significantly improves cardiac function and myocardial infarction area, increases nitric oxide, endothelial nitric oxide synthase and ATPase (Na⁺-K⁺-ATPase and Ca²⁺-Mg²⁺-ATPase) activity and decreases levels of oxygen stress, myocardial enzymes and endothelin-1. Notably, HBO and diltiazem preconditioning significantly increased Bcl-2 protein expression and decreased Bax protein and caspase-3 mRNA expression. Conclusions: These data indicate that combination therapy protected against heart MIRI by reducing oxygen stress damage, correcting energy metabolism, improving endothelial function and inhibiting cell apoptosis.

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“…The lower levels of roS indicated by dHe oxidation may have resulted from increased Sod and caT expression. although the mechanisms by which HBo therapy induces an antioxidant response remain unclear, it has been reported to involve a nrf2-dependent effect (43,44) triggered in a pro-oxidizing environment (31). indeed, we observed that HBO decreased the GSH/GSSG ratio, confirming such nrf2-inducing conditions.…”

Section: Discussionmentioning

confidence: 99%

Hyperbaric oxygenation improves redox control and reduces mortality in the acute phase of myocardial infarction in a rat model

et al. 2020

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among the mechanisms of action of hyperbaric oxygenation (HBo), the chance of reducing injury by interfering with the mechanisms of redox homeostasis in the heart leads to the possibility of extending the period of viability of the myocardium at risk. This would benefit late interventions for reperfusion to the ischemic area. The objective of the present study was to investigate the changes in the redox system associated with HBO therapy maintained during the first hour after coronary occlusion in an acute myocardial infarction (Mi) rat model. Surviving male rats (n=105) were randomly assigned to one of three groups: Sham (SH=26), myocardial infarction (Mi=45) and infarction+hyperbaric therapy (HBo=34, 1 h at 2.5 atm). after 90 min of coronary occlusion, a sample of the heart was collected for western blot analysis of total protein levels of superoxide dismutase, catalase, peroxiredoxin and 3-nitrotyrosine. Glutathione was measured by enzyme-linked immunosorbent assay (eliSa). The detection of the superoxide radical anion was carried out by oxidation of dihydroethidium analyzed with confocal microscopy. The mortality rate of the MI group was significantly higher than that of the HBO group. no difference was noted in the myocardial infarction size. The oxidized/reduced glutathione ratio and peroxiredoxin were significantly higher in the SH and MI when compared to the HBo group. Superoxide dismutase enzymes and catalase were significantly higher in the HBO group compared to the MI and SH groups. 3-nitrotyrosine and the superoxide radical were significantly lower in the HBO group compared to these in the Mi and SH groups. These data demonstrated that hyperbaric oxygenation therapy decreased mortality by improving redox control in the hearts of rats in the acute phase of myocardial infarction.

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Hyperbaric Oxygen Preconditioning Attenuates Myocardium Ischemia-Reperfusion Injury Through Upregulation of Heme Oxygenase 1 Expression

Abstract: These data present a novel signaling mechanism by which hyperbaric oxygen preconditioning protects myocardium ischemia-reperfusion injury via PI3K/Akt/Nrf2-dependent antioxidant defensive system.

Cited by 41 publications

References 54 publications

Naringin protects against anoxia/reoxygenation-induced apoptosis in H9c2 cells via the Nrf2 signaling pathway

Naringin protects against anoxia/reoxygenation-induced apoptosis in H9c2 cells via the Nrf2 signaling pathway

Cardioprotective Effects of Combined Therapy with Hyperbaric Oxygen and Diltiazem Pretreatment on Myocardial Ischemia-Reperfusion Injury in Rats

Hyperbaric oxygenation improves redox control and reduces mortality in the acute phase of myocardial infarction in a rat model

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