Corrigendum to "High-Dose Polymerized Hemoglobin Fails to Alleviate Cardiac Ischemia/Reperfusion Injury due to Induction of Oxidative Damage in Coronary Artery".
Ontology highlight
ABSTRACT:
SUBMITTER: Yang Q
PROVIDER: S-EPMC6425291 | biostudies-literature | 2019
REPOSITORIES: biostudies-literature
Publications
Corrigendum to "High-Dose Polymerized Hemoglobin Fails to Alleviate Cardiac Ischemia/Reperfusion Injury due to Induction of Oxidative Damage in Coronary Artery".
Yang Qian Q Wu Wei W Li Qian Q Chen Chan C Zhou Ronghua R Qiu Yanhua Y Luo Ming M Tan Zhaoxia Z Li Shen S Chen Gang G Zhou Wentao W Liu Jiaxin J Yang Chengmin C Liu Jin J Li Tao T
Oxidative medicine and cellular longevity 20190304
[This corrects the article DOI: 10.1155/2015/125106.]. ...[more]
Similar Datasets
Project description:Acute kidney injury is a leading contributor to morbidity and mortality in the ageing population. Proteotoxic stress response pathways have been suggested to contribute to the development of acute renal injury. Recent evidence suggests that increased synthesis of N-glycan precursors in the hexosamine pathway as well as feeding of animals with aminosugars produced in the hexosamine pathway may increase stress resistance through reducing proteotoxic stress and alleviate pathology in model organisms. As feeding of the hexosamine pathway metabolite glucosamine to aged mice increased their life expectancy we tested whether supplementation of this aminosugar may also protect mice from acute kidney injury after renal ischemia and reperfusion. Animals were fed for 4 weeks ad libitum with standard chow or standard chow supplemented with 0.5% N-acetylglucosamine. Preconditioning with caloric restriction for four weeks prior to surgery served as a positive control for protective dietary effects. Whereas caloric restriction demonstrated the known protective effect both on renal function as well as survival in the treated animals, glucosamine supplementation failed to promote any protection from ischemia-reperfusion injury. These data show that although hexosamine pathway metabolites have a proven role in enhancing protein quality control and survival in model organisms oral glucosamine supplementation at moderate doses that would be amenable to humans does not promote protection from ischemia-reperfusion injury of the kidney.
| S-EPMC4996512 | biostudies-literature
Project description:(±)-Anastatins A and B are flavonoids isolated from Anastatica hierochuntica. In a previous study, twenty-four di- and tri-substituted novel derivatives of anastatins were designed and their preliminary antioxidant activities were evaluated. In the present study, the protective effect of myocardial ischemia-reperfusion (I/R) and the systematic antioxidant capacity of 24 derivatives were further studied. Compound 13 was the most potent among all the compounds studied, which increased the survival of H9c2 cells to 80.82%. The antioxidant capability of compound 13 was evaluated in ferric reducing antioxidant power, 2,2'-azino-bis (3-ethylbenzothiazoline-6-sulfonic acid) radical scavenging, and 2,2-diphenyl-1-picrylhydrazyl assays. It was observed that compound 13 significantly reduced infarcted areas and improved histopathological and electrocardiogram changes in rats with myocardial I/R injury. Moreover, compound 13 decreased the leakage rates of serum lactate dehydrogenase, creatine kinase, and malonyldialdehyde from rat myocardial tissues and increased the level of glutathione and superoxide dismutase activities following myocardial I/R injury in rats. Taken together, we concluded that compound 13 had potent cardioprotective effects against myocardial I/R injury both in vitro and in vivo owing to its extensive antioxidant activities.
| S-EPMC8399290 | biostudies-literature
Project description:Hepatic ischemia/reperfusion (I/R) injury is an important cause of liver function impairment following liver surgery. The ubiquitin-proteasome system (UPS) plays a crucial role in protein quality control and has substantial impact on the hepatic I/R process. Although OTU deubiquitinase 1 (OTUD1) is involved in diverse biological processes, its specific functional implications in hepatic I/R are not yet fully understood. This study demonstrates that OTUD1 alleviates oxidative stress, apoptosis, and inflammation induced by hepatic I/R injury. Mechanistically, OTUD1 deubiquitinates and activates nuclear factor erythroid 2-related factor 2 (NRF2) through its catalytic site cysteine 320 residue and ETGE motif, thereby attenuating hepatic I/R injury. Additionally, administration of a short peptide containing the ETGE motif significantly mitigates hepatic I/R injury in mice. Overall, our study elucidates the mechanism and role of OTUD1 in ameliorating hepatic I/R injury, providing a theoretical basis for potential treatment using ETGE-peptide.
| S-EPMC11340619 | biostudies-literature
Project description:Hepatic ischemia-reperfusion (I/R) injury frequently occurs during the perioperative phase of liver surgery. Inappropriate activation of STING signaling can trigger excessive inflammation response to aggravate hepatic I/R injury. Dimethyl fumarate (DMF) is an FDA-approved immunomodulatory drug used to treat multiple sclerosis and psoriasis due to its notable anti-inflammation properties. However, the mechanism and targets of DMF in immunomodulation remain unclear. Here, we found that DMF suppresses cGAS-STING activation induced by HSV-1, hering testis DNA, and mitochondrial DNA in a variety of cells. DMF significantly reduces hepatic I/R injury and inhibits cGAS-STING pathway activation in mice. The alleviating effect of DMF on hepatic I/R injury was negligible in STING-knockout mice. Mechanistically, DMF directly inhibits STING activation via an autophagy-independent pathway, and the immunocoprecipitation experiment showed that DMF inhibited STING recruitment of downstream TBK1 and IRF3. Our study found that DMF protects liver I/R injury by inhibiting the STING pathway and may be a potential target of this disease.
| S-EPMC11773390 | biostudies-literature
Project description:Peroxisome proliferator-activated receptor (PPAR)-gamma modulates substrate metabolism and inflammatory responses. In experimental rats subjected to myocardial ischemia-reperfusion (I/R), thiazolidinedione PPAR-gamma activators reduce infarct size and preserve left ventricular function. Troglitazone is the only PPAR-gamma activator that has been shown to be protective in I/R in large animals. However, because troglitazone contains both alpha-tocopherol and thiazolidinedione moieties, whether PPAR-gamma activation per se is protective in myocardial I/R in large animals remains uncertain. To address this question, 56 pigs were treated orally for 8 wk with troglitazone (75 mg x kg(-1) x day(-1)), rosiglitazone (3 mg x kg(-1) x day(-1)), or alpha-tocopherol (73 mg x kg(-1) x day(-1), equimolar to troglitazone dose) or received no treatment. Pigs were then anesthetized and subjected to 90 min of low-flow regional myocardial ischemia and 90 min of reperfusion. Myocardial expression of PPAR-gamma, determined by ribonuclease protection assay, increased with troglitazone and rosiglitazone compared with no treatment. Rosiglitazone had no significant effect on myocardial contractile function (Frank-Starling relations), substrate uptake, or expression of proinflammatory cytokines during I/R compared with untreated pigs. In contrast, preservation of myocardial contractile function and lactate uptake were greater and cytokine expression was attenuated in pigs treated with troglitazone or alpha-tocopherol compared with untreated pigs. Multivariate analysis indicated that presence of an alpha-tocopherol, but not a thiazolidinedione, moiety in the test compound was significantly related to greater contractile function and lactate uptake and lower cytokine expression during I/R. We conclude that PPAR-gamma activation is not protective in a porcine model of myocardial I/R. Protective effects of troglitazone are attributable to its alpha-tocopherol moiety. These findings, in conjunction with prior rat studies, suggest interspecies differences in the response to PPAR-gamma activation in the heart.
| S-EPMC3633522 | biostudies-literature
Project description:Ischemic postconditioning (IPO) attenuates hepatic ischemia/reperfusion (I/R) injury. However, little is known about the underlying biological pathophysiology, which could be, at least in part, informed by exploring the transcriptomic changes using next-generation RNA sequencing (RNA-Seq). In this study, 18 mice (C57BL/6) were involved and randomly assigned to three groups: normal (n=6), I/R (n=6, subjected to 70% hepatic I/R), and IR+IPO (n=6, applying IPO to mice with I/R injury). We randomly selected 3 mice per group and extracted their liver tissues for next-generation RNA-Seq. We performed a bioinformatics analysis for two comparisons: normal vs. I/R and I/R vs. IR+IPO. From the analysis, 2416 differentially expressed genes (DEGs) were identified (p < 0.05 and fold change ≥ 1.5). Gene ontology (GO) analysis revealed that these genes were mainly related to cellular metabolic processes, nucleic acids and protein binding processes. The enriched Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways for the DEGs were the mitogen-activated protein kinase (MAPK), IL-17 signalling pathway, regulating pluripotency of stem cells, and insulin resistance pathway. Validation of 12 selected DEGs by qRT-PCR showed that Cyr61, Atf3, Nr4a1, Gdf15, Osgin1, Egr1, Epha2, Dusp1, Dusp6, Gadd45a and Gadd45b were significantly amplified. Finally, a protein-protein interaction (PPI) network constructed to determine interactions of these 11 DEGs. In summary, by exploring gene expression profiling in regard to hepatic I/R and IPO using next-generation RNA-Seq, we suggested a few progression-related genes and pathways, providing some clues for future experimental research.
| S-EPMC6367534 | biostudies-literature
Project description:Extracellular vesicles (EVs) produced by anoxia-preconditioned mesenchymal stem cells (MSCs) may afford greater cardioprotection against myocardial ischemia-reperfusion injury (MIRI) than EVs derived from normoxic MSCs. Here, we isolated EVs from mouse adipose-derived MSCs (ADSCs) subjected to anoxia preconditioning or normoxia and evaluated their ability to promote survival of mouse cardiomyocytes following MIRI in vivo and anoxia/reoxygenation (AR) in vitro. Injection of anoxia-preconditioned ADSC EVs (Int-EVs) reduced both infarct size and cardiomyocyte apoptosis to a greater extent than normoxic ADSC EVs (NC-EVs) in mice subjected to MIRI. Sequencing EV-associated miRNAs revealed differential upregulation of ten miRNAs predicted to bind thioredoxin-interacting protein (TXNIP), an inflammasome- and pyroptosis-related protein. We confirmed direct binding of miRNA224-5p, the most upregulated miRNA in Int-EVs, to TXNIP and asserted through western blotting and apoptosis assays a critical protective role for this miRNA against AR-induced cardiomyocyte death. Our results suggest that ischemia-reperfusion triggers TXNIP-induced inflammasome activation in cardiomyocytes, which leads to apoptosis rather than pyroptosis due to low basal levels of the pyroptosis executioner protein gasdermin D in these cells. The antiapoptotic effect of EV-associated miRNA224-5p would in turn result from TXNIP downregulation, which prevents caspase-1-mediated degradation of GATA4 and sustains the expression of Bcl-2.
| S-EPMC7950238 | biostudies-literature
Project description:Clinically, antioxidant therapy is a potential strategy for myocardial ischemia-reperfusion injury (MI/RI), a common complication of acute myocardial ischemia. The H-D-Arg-Dmt-Ly-Phe-NH2 (SS31) peptide is shown to have amazing antioxidant properties, but its utilization is limited by the peptide characteristics, such as the destruction by proteases and rapid metabolism. Silica nanoparticles (MSNs) comprise an excellent material for peptide delivery, owing to the protection effect relating to peptides. Moreover, platelet membrane (PLTM) is shown to be advantageous as a coat for nanosystems because of its specific protein composition, such that a PLTM-coated nanosystem has a stealth effect in vivo, able to target injury in the cardiovascular system. Based on this feature, we designed and prepared a novel nanocarrier to target SS31 delivery. This carrier is encapsulated by a platelet membrane and loaded with SS31 peptide into MSNs. The results reveal that this delivery system can target SS31 to the injured cardiovascular site, exert antioxidant function, and alleviate MI/RI.
| S-EPMC9624354 | biostudies-literature
Project description:[This corrects the article DOI: 10.3389/fphar.2022.1043945.].
| S-EPMC10115130 | biostudies-literature
Project description:Ischemia-reperfusion injury (IRI) is a major cause of morbidity and mortality following conventional lung transplantation and warm ischemia may limit success of transplanting lungs from non-heart-beating donors. We sought to determine alterations in gene expression in rat lung tissue subjected to warm ischemia in vivo followed by reperfusion. Keywords: time course
2019-04-30 | GSE9634 | GEO