Search results for "Reperfusion"

showing 10 items of 210 documents

Thyroid stem cells: phenotypic properties, differentiation, potential and regulation by bone morphogenetic proteins

2006

Ischemia-reperfusion injury, a clinical problem during cardiac surgery, involves worsened adenosine trisphosphate (ATP) generation and damage to the heart. We studied carbon monoxide ( CO) pretreatment, proven valuable in rodents but not previously tested in large animals, for its effects on pig hearts subjected to cardiopulmonary bypass with cardioplegic arrest. Hearts of CO-treated pigs showed significantly higher ATP and phosphocreatine levels, less interstitial edema, and apoptosis of cardiomyocytes and required fewer defibrillations after bypass. We conclude that treatment with CO improves the energy status, prevents edema formation and apoptosis, and facilitates recovery in a clinical…

Ischemia-reperfusion
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Remote Ischemic Preconditioning Decreases Oxidative Lung Damage After Pulmonary Lobectomy

2017

BACKGROUND:During lobectomy in patients with lung cancer, the operated lung is often collapsed and hypoperfused. Ischemia/reperfusion injury may then occur when the lung is re-expanded. We hypothesized that remote ischemic preconditioning (RIPC) would decrease oxidative lung damage and improve gas e

Lungbusiness.industryIschemiaHemodynamicsrespiratory system030204 cardiovascular system & hematologyLung injurymedicine.diseasemedicine.disease_causerespiratory tract diseases03 medical and health sciences0302 clinical medicineAnesthesiology and Pain Medicinemedicine.anatomical_structure030228 respiratory systemAnesthesiamedicineIschemic preconditioningbusinessLung cancerReperfusion injuryOxidative stressAnesthesia & Analgesia
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CSF-1 signals directly to renal tubular epithelial cells to mediate repair in mice

2009

金沢大学医薬保健研究域医学系

Macrophage colony-stimulating factorPathologymedicine.medical_specialtymedicine.medical_treatmenteducation030232 urology & nephrologyApoptosisReceptor Macrophage Colony-Stimulating FactorBiology03 medical and health sciencesParacrine signallingMice0302 clinical medicineFibrosismedicineAnimalsHumansRegenerationAutocrine signalling030304 developmental biologyCell Proliferation0303 health sciencesMice Inbred C3HGrowth factorMacrophage Colony-Stimulating FactorMacrophageshemic and immune systemsEpithelial CellsGeneral Medicinemedicine.diseaseFibrosis3. Good healthKidney TubulesIntegrin alpha MApoptosisReperfusion Injurybiology.proteinCancer researchReperfusion injurytissuesResearch Article
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Allopurinol Protective Effect of Renal Ischemia by Downregulating TNF-α, IL-1β, and IL-6 Response

2016

Allopurinol is a well-known antioxidant that protects tissue against ischemia and reperfusion injury, blocking purine catabolism, and possibly reducing TNF-α and other cytokines. It also plays a significant role in reducing the inflammatory processes by inhibiting chemotaxis and other inflammatory mediators. The objective of this study was to define the role of allopurinol regarding kidney ischemic injury particularly as to its effect on inflammatory molecules such as TNF-α, IL-1β, and IL-6 response. One hundred and twenty five rats were subjected to warm renal ischemia. Five more animals were included as sham. Animal survival and plasma levels of lipid peroxidation, myeloperoxidase, lactat…

Male0301 basic medicineAllopurinolDrug Evaluation PreclinicalIschemiaAllopurinolPharmacologyKidneyGout SuppressantsLipid peroxidation03 medical and health scienceschemistry.chemical_compound0302 clinical medicineLactate dehydrogenaseAnimalsMedicineRats WistarKidneybiologyRenal ischemiaInterleukin-6Tumor Necrosis Factor-alphabusiness.industryInterleukin-18Acute Kidney Injurymedicine.disease030104 developmental biologymedicine.anatomical_structurechemistryReperfusion Injury030220 oncology & carcinogenesisMyeloperoxidaseImmunologybiology.proteinSurgerybusinessReperfusion injurymedicine.drugJournal of Investigative Surgery
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Telmisartan cardioprotects from the ischaemic/hypoxic damage through a miR‐1‐dependent pathway

2019

The aim of this study was to investigate whether telmisartan protects the heart from the ischaemia/reperfusion damage through a local microRNA-1 modulation. Studies on the myocardial ischaemia/reperfusion injury in vivo and on the cardiomyocyte hypoxia/reoxygenation damage in vitro were done. In vivo, male Sprague-Dawley rats administered for 3 weeks with telmisartan 12 mg/kg/d by gastric gavage underwent ischaemia/reperfusion of the left descending coronary artery. In these rats, infarct size measurement, ELISA, immunohistochemistry (IHC) and reverse transcriptase real-time polymerase chain reaction showed that expressions of connexin 43, potassium voltage-gated channel subfamily Q member …

Male0301 basic medicineCell SurvivalMyocardial InfarctionIschemiaConnexinMyocardial Reperfusion InjuryPharmacologymiR‐1telmisartanCell Lineconnexin 43Rats Sprague-Dawleyhypoxic H9c2 cells03 medical and health sciences0302 clinical medicineIn vivomedicineAnimalsBcl-2Myocytes CardiacKCNQ1ChemistryBcl‐2Original ArticlesCell BiologyTransfectionHypoxia (medical)medicine.diseasemiR-1Cell HypoxiaIn vitroRatsMicroRNAsmyocardial ischaemia/reperfusion030104 developmental biologyProto-Oncogene Proteins c-bcl-2030220 oncology & carcinogenesisKCNQ1 Potassium ChannelMolecular Medicinehypoxic H9c2 cellOriginal Articlemedicine.symptomTelmisartanReperfusion injurymedicine.drugJournal of Cellular and Molecular Medicine
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Molecular mechanisms mediating the neuroprotective role of the selective estrogen receptor modulator, bazedoxifene, in acute ischemic stroke: A compa…

2017

As the knowledge on the estrogenic system in the brain grows, the possibilities to modulate it in order to afford further neuroprotection in brain damaging disorders so do it. We have previously demonstrated the ability of the selective estrogen receptor modulator, bazedoxifene (BZA), to reduce experimental ischemic brain damage. The present study has been designed to gain insight into the molecular mechanisms involved in such a neuroprotective action by investigating: 1) stroke-induced apoptotic cell death; 2) expression of estrogen receptors (ER) ERα, ERβ and the G-protein coupled estrogen receptor (GPER); and 3) modulation of MAPK/ ERK1/2 and PI3K/Akt signaling pathways. For comparison, …

Male0301 basic medicineMAPK/ERK pathwayIndolesSignaling pathwaysEndocrinology Diabetes and MetabolismClinical BiochemistryEstrogen receptorApoptosisEstrogen receptorsSecond Messenger SystemsBiochemistryBrain IschemiaReceptors G-Protein-Coupled0302 clinical medicineEndocrinologyPhosphatidylinositol PhosphatesCerebral CortexNeuronsEstradiolNeuroprotectionStrokeNeuroprotective AgentsSelective estrogen receptor modulatorReperfusion InjuryMolecular MedicineSelective estrogen receptor modulatorsGPERmedicine.medical_specialtyMAP Kinase Signaling Systemmedicine.drug_classAcute ischemic strokeNerve Tissue ProteinsBazedoxifeneBiologyNeuroprotection03 medical and health sciencesInternal medicinemedicineAnimalsEstrogen Receptor betaRats WistarMolecular BiologyProtein kinase BPI3K/AKT/mTOR pathwayEstrogen Receptor alphaEstrogensCell BiologyEstrogen030104 developmental biologyEndocrinologyEstrogen030217 neurology & neurosurgeryThe Journal of Steroid Biochemistry and Molecular Biology
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Investigating and re-evaluating the role of glycogen synthase kinase 3 beta kinase as a molecular target for cardioprotection by using novel pharmaco…

2019

Aims Glycogen synthase kinase 3 beta (GSK3β) link with the mitochondrial Permeability Transition Pore (mPTP) in cardioprotection is debated. We investigated the role of GSK3β in ischaemia (I)/reperfusion (R) injury using pharmacological tools. Methods and results Infarct size using the GSK3β inhibitor BIO (6-bromoindirubin-3'-oxime) and several novel analogues (MLS2776-MLS2779) was determined in anaesthetized rabbits and mice. In myocardial tissue GSK3β inhibition and the specificity of the compounds was tested. The mechanism of protection focused on autophagy-related proteins. GSK3β localization was determined in subsarcolemmal (SSM) and interfibrillar mitochondria (IFM) isolated from Lang…

Male0301 basic medicinePhysiologyMyocardial InfarctionAutophagy-Related ProteinsMyocardial Reperfusion Injury030204 cardiovascular system & hematologyMitochondrionPharmacologyMitochondrial Membrane Transport ProteinsMitochondria HeartStructure-Activity Relationship03 medical and health scienceschemistry.chemical_compound0302 clinical medicineReperfusion therapyPhysiology (medical)AnimalsMyocytes CardiacProtein Kinase InhibitorsGSK3BMice Knockoutchemistry.chemical_classificationCardioprotectionReactive oxygen speciesGlycogen Synthase Kinase 3 betaMolecular StructureMitochondrial Permeability Transition PoreChemistryKinaseMPTPIsolated Heart PreparationMice Inbred C57BLDisease Models Animal030104 developmental biologyMitochondrial permeability transition poreFemaleRabbitsCardiology and Cardiovascular MedicineCyclophilin DSignal TransductionCardiovascular Research
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Faim2 contributes to neuroprotection by erythropoietin in transient brain ischemia.

2018

Delayed cell death in the penumbra region of acute ischemic stroke occurs through apoptotic mechanisms, making it amenable to therapeutic interventions. Fas/CD95 mediates apoptotic cell death in response to external stimuli. In mature neurons, Fas/CD95 signaling is modulated by Fas-apoptotic inhibitory molecule 2 (Faim2), which reduces cell death in animal models of stroke, meningitis, and Parkinson disease. Erythropoietin (EPO) has been studied as a therapeutic strategy in ischemic stroke. Erythropoietin stimulates the phosphatidylinositol-3 kinase/Akt (PI3K/Akt) pathway, which regulates Faim2 expression. Therefore, up-regulation of Faim2 may contribute to neuroprotection by EPO. Male Faim…

Male0301 basic medicinemetabolism [Apoptosis Regulatory Proteins]FAIM2 protein humanlifeguard protein mouseIschemiaNerve Tissue Proteinspathology [Ischemic Attack Transient]physiology [Neuroprotection]PharmacologyBiochemistryNeuroprotectionmetabolism [Erythropoietin]metabolism [Ischemic Attack Transient]Brain ischemiaMice03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicinemedicineAnimalsHumansddc:610ErythropoietinStrokeProtein kinase BPI3K/AKT/mTOR pathwayAgedpharmacology [Erythropoietin]Mice Knockoutmetabolism [Nerve Tissue Proteins]business.industryPenumbraMembrane ProteinsMiddle Agedmedicine.diseaseNeuroprotection030104 developmental biologyIschemic Attack TransientErythropoietinphysiopathology [Ischemic Attack Transient]FemaleDose-dependency ; Erythropoietin ; Fas-apoptotic Inhibitory Molecule 2 ; Ischemia-reperfusion ; Neuroprotection ; StrokeApoptosis Regulatory Proteinsbusinessmetabolism [Membrane Proteins]030217 neurology & neurosurgerymedicine.drug
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Systemic blockade of ACVR2B ligands protects myocardium from acute ischemia-reperfusion injury

2019

Activin A and myostatin, members of the transforming growth factor (TGF)-β superfamily of secreted factors, are potent negative regulators of muscle growth, but their contribution to myocardial ischemia-reperfusion (IR) injury is not known. The aim of this study was to investigate if activin 2B (ACVR2B) receptor ligands contribute to myocardial IR injury. Mice were treated with soluble ACVR2B decoy receptor (ACVR2B-Fc) and subjected to myocardial ischemia followed by reperfusion for 6 or 24 h. Systemic blockade of ACVR2B ligands by ACVR2B-Fc was protective against cardiac IR injury, as evidenced by reduced infarcted area, apoptosis, and autophagy and better preserved LV systolic function fo…

MaleActivin Receptors Type IIiskemialihaksetSmad2 ProteinMyostatinPharmacologyMice0302 clinical medicineDrug DiscoverykasvutekijätMyocytes CardiacCardioprotection0303 health sciences318 Medical biotechnologybiologysydänactivins1184 Genetics developmental biology physiologyII RECEPTORS3. Good health030220 oncology & carcinogenesisMolecular MedicineOriginal ArticleSignal TransductionCardiac function curvegrowth differentiation factorsProgrammed cell deathBLOCKINGischemia-reperfusion injuryIschemiaMyocardial Reperfusion InjuryMASSta311103 medical and health sciencesMYOSTATIN-KNOCKOUTCARDIOPROTECTIONGeneticsmedicineAnimalsMolecular Biologylihassolut030304 developmental biologyPharmacologySKELETAL-MUSCLE GROWTHbusiness.industryMyocardiumFOLLISTATINMyostatinmedicine.diseaseACVR2BMice Inbred C57BLACTIVIN-AGDF11GDF11biology.protein3111 BiomedicineproteiinitbusinessReperfusion injuryDIFFERENTIATION FACTOR 11ACVR2BTranscription Factors
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Carbon Monoxide Protects Against Ischemia-reperfusion Injury in Vitro via Antioxidant Properties

2012

Carbon monoxide (CO) is believed to mediate many of the cytoprotective effects attributed to the activation of heme oxygenase (HO-1), the enzyme responsible for CO production. Recently, the study of CO-releasing molecules (CO-RMs) has provided a new approach for the delivery of CO. In the present study, we examined whether the cardioprotective properties of CO-RM2 in isolated rat hearts subjected to an ischemia-reperfusion (I/R) sequence were associated with the presence of CO. In addition, the antioxidant properties of CO-RM2 were evaluated. In hearts pretreated with CO-RM2, the improvement in contractile function at the end of the reperfusion period after 20 min of global total ischemia w…

MaleAntioxidantCardiotonic AgentsTime FactorsPhysiologymedicine.medical_treatmentIschemiaPharmacologyIn Vitro Techniquesmedicine.disease_causeAntioxidantsVentricular Function Left03 medical and health scienceschemistry.chemical_compound0302 clinical medicine[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemSuperoxidesEthidiummedicineOrganometallic CompoundsAnimalsRats WistarComputingMilieux_MISCELLANEOUS030304 developmental biologychemistry.chemical_classification0303 health sciencesCarbon MonoxideL-Lactate DehydrogenaseSuperoxideHeartmedicine.diseaseMyocardial ContractionIn vitroRats[SDV.MHEP.CSC] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemHeme oxygenaseOxidative StressEnzymechemistryBiochemistry030220 oncology & carcinogenesisReperfusion InjuryReperfusion injuryOxidative stress
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