• Myocardial ischemia-reperfusion (I/R) injury is an important health concern in myocardial infarction and situations such as angioplasty and cardiac surgeries. (usask.ca)
  • Worldwide morbidity and mortality from acute myocardial infarction (AMI) and related heart failure remain high. (hindawi.com)
  • Among clinical emergency events, ST-segment elevation (STE) or the non-STE electrocardiogram diagnosis of acute myocardial infarction (AMI) is particularly common worldwide, with a staggering number of annual first episodes as well as recurrent ones [ 1 ]. (hindawi.com)
  • GRh2 reduced the area of myocardial infarction and the histological changes in the myocardium and improved cardiac functions. (spandidos-publications.com)
  • The abnormal morphology and dysfunction of mitochondria have been proven as the principal mechanisms in the pathogenesis of cardiovascular diseases, such as heart failure, myocardial infarction, atherosclerosis, and hypertension ( 4 - 6 ). (frontiersin.org)
  • The clinical unit is located at the Department of Cardiology and focuses on prospective studies of patients with ST-elevation myocardial infarction (STEMI) who are treated with primary percutaneous coronary intervention. (gu.se)
  • Injury models to study cardiac remodeling in the mouse: myocardial infarction and ischemia-reperfusion. (omeka.net)
  • Following myocardial infarction (MI), elderly patients have a poorer prognosis than younger patients, which may be linked to increased coronary microvessel susceptibility to injury. (jci.org)
  • Myocardial infarction (MI) denotes the death of cardiac myocytes due to extended ischemia. (aku.edu)
  • MI model was also associated with increase in the neutrophil polymorphs number in the infarction related myocardium as compared to the re-perfused myocardium. (aku.edu)
  • Hashmi, S & Al-Salam, S 2015, ' Acute myocardial infarction and myocardial ischemia-reperfusion injury: A comparison ', International Journal of Clinical and Experimental Pathology , vol. 8, no. 8, pp. 8786-8796. (uaeu.ac.ae)
  • The administration of bone marrow-derived mesenchymal stem cells (BMSCs) is emerging as a promising approach for I/R injury-induced myocardial infarction due to its multiple differentiation potential(7, 8). (researchsquare.com)
  • B. Rosiglitazone, a peroxisome proliferator-activated receptor-gamma ligand, reduces infarction volume and neurological deficits in an embolic model of stroke. (ac.ir)
  • Acute myocardial infarction (MI) is a global issue with high incidence and mortality. (edu.iq)
  • Rapid recovery of the blocked coronary flow represents the most effective strategy to reduce the size of myocardial infarction and improve the cardiac function. (edu.iq)
  • Result: Compared with the experimental group, Salvia miltiorrhiza injection ameliorated myocardial ischemia-reperfusion injury, and decreased the infarction area seen in Evans/TTC staining. (archive.org)
  • When ischemia is severe and prolonged, it causes myocyte death and results in loss of contractile function and tissue infarction. (medscape.com)
  • Schematic representation of infarction (cell death), chronic ischemia with contractile dysfunction (hibernating myocardium), and transient ischemia (stunned myocardium) with restored blood flow with transient contractile dysfunction. (medscape.com)
  • Stroke and myocardial infarction are among the most common causes of mortality and disability in the world. (cdc.gov)
  • The Canadian Cardiovascular Society (CCS) has developed a four-stage classification of acute atherothrombotic myocardial infarction (MI) based on the severity of the injury to the myocardium. (medscape.com)
  • Hypercholesterolemia causes endothelial and myocardial dysfunction, as well as aggravates ischemia/reperfusion (I/R)-induced myocardial injury. (nih.gov)
  • Pretreating the rats with simvastatin 18 hour prior to the induction of ischemiareperfusion has been shown to reduce cardiac dysfunction and improve coronary flow [ 7 ]. (ac.ir)
  • The role of cardiac proteasome dysfunction during I/R and the perspective to diminish I/R injury by manipulating proteasome function remain unclear. (elsevierpure.com)
  • In heart transplantation, donor hearts inevitably suffer from ischemia/reperfusion (I/R) injury, which leads to primary graft dysfunction and affects patients' survival rate. (researchsquare.com)
  • All of these factors are known to result in myocardial apoptosis(5) and the acceleration of allograft rejection or chronic allograft dysfunction. (researchsquare.com)
  • A wealth of studies now confirm that PQQ's cell-signaling activity translates into substantial protection against degenerative and age-related conditions, such as mitochondrial dysfunction, 1 heart degeneration, 18-20 brain injury, and cognitive decline. (lifeextension.com)
  • Blood platelets dysfunction was induced after myocardial ischemia-reperfusion, and the level of PECAM-1 increased. (archive.org)
  • Cardiac cells that survive this first wave of injuries will often have their mitochondrial functions compromised, and this can lead to further dysfunction and even cellular death. (prohealth.com)
  • Stunned myocardium is myocardium that suffers transient reversible myocardial contractile dysfunction that is caused by acute ischemia during which the blood supply is almost completely restored by reperfusion, with no metabolic deterioration. (medscape.com)
  • The term hibernating myocardium is also used to indicate chronic myocardial contractile dysfunction due to ischemia, in which there is reduced coronary blood flow at rest and increased myocardial demand results in impaired contractility. (medscape.com)
  • Finding all 3 entities in the same patient with chronic myocardial dysfunction is not uncommon (see the image above). (medscape.com)
  • Myocardial I/R injury may induce cell apoptosis and autophagy by activating oxidative stress and upregulating inflammatory mediators, ultimately resulting in irreversible fibrotic damage ( 3 ). (spandidos-publications.com)
  • The pathophysiological nature of MIRI is the short-term disturbance of myocardial energy and metabolism caused by reflow after ischemia and hypoxia in the coronary artery and the dynamic changes in apoptosis and the prosurvival signaling pathways in response to related injury factors. (hindawi.com)
  • Dexmedetomidine pretreatment can obviously relieve myocardial ischemia-reperfusion injury and cardiomyocyte apoptosis in rats probably by activating the Janus kinase 2/signal transducers and activators of transcription 3 signaling pathway. (ijpsonline.com)
  • Upregulation of Fas expression in myocardial ischemia-reperfusion can induce cardiomyocyte apoptosis, and atorvastatin can significantly inhibit cardiomyocyte apoptosis by inhibiting Fas expression. (ac.ir)
  • Apoptosis of the cardiomyocytes has been demonstrated in animal models with coronary artery occlusion [ 1 ], and experimental evidence suggests that myocardial cells are able to undergo apoptosis during ischemia followed by reperfusion [ 2 ]. (ac.ir)
  • Both ischemic and reperfused rat myocardium can undergo apoptotic cell death, however the myocardium, which is subjected to ischemia followed by reperfusion, undergoes accelerated apoptosis [ 3 ]. (ac.ir)
  • In conclusion, myocardial damage in MI is mainly due to ischemic necrosis and inflammatory mechanisms while apoptosis is the main mechanism of cell death in IR in addition to limited ischemic necrosis. (aku.edu)
  • 6. Xing B, Chen H, Zhang M, Zhao D, Jiang R, Liu X, Zhang S. Ischemic postconditioning inhibits apoptosis after focal cerebral ischemia/reperfusion injury in the rat. (ac.ir)
  • 7. Yuan Y, Guo Q, Ye Z, Pingping X, Wang N, Song Z. Ischemic postconditioning protects brain from ischemia/reperfusion injury by attenuating endoplasmic reticulum stress-induced apoptosis through PI3K-Akt pathway. (ac.ir)
  • Also, curcumin reduces cell apoptosis induced by myocardial IRI, curcumin reduces cell apoptosis induced by myocardial IRI and activates the Nrf-2/HO-1 signaling pathway during myocardial. (edu.iq)
  • The most effective early treatment for reducing AMI injury and limiting the infarcted myocardium is timely coronary revascularization using thrombolytic therapy or primary percutaneous coronary intervention (PPCI) [ 2 - 4 ]. (hindawi.com)
  • This coupled comorbidity of pathological ischemia and therapeutic reinjury of infarcted myocardium, namely, myocardial ischemia-reperfusion injury (MIRI), is particularly refractory to treatment [ 4 , 5 ]. (hindawi.com)
  • During injury stimulation, the major effects on the cardiac function may be those involving mitochondria-dominated events along with potential nucleus-governed genetic/epigenetic alternations within the cardiomyocytes as well as the macrophage-led inflammation and T-cell-led immune responses underlying the myocardium-vessel interactive cascade. (hindawi.com)
  • However, whether GRh2 has a protective effect on ischaemia/reperfusion (I/R) in the myocardium has yet to be elucidated. (spandidos-publications.com)
  • These pleiotropic effects thus have a major role in protecting the myocardium against ischemic injury. (ac.ir)
  • 2002 - defended ahead of time his PhD thesis in Pathologic Physiology entitled «Comparative evaluation of the cardioprotective efficacy of local and distant ischemic adaptation of the myocardium» dedicated to myocardial protection against ischemia injury in the experiment. (almazovcentre.ru)
  • Reperfusion has the potential to salvage ischemic myocardium but paradoxically can cause injury, a phenomenon called as 'reperfusion injury' (IR). (aku.edu)
  • Our IR model showed enhanced pro-apoptotic mediators like cleaved caspase-3 (P=0.005) and cytochrome c in the myocardium as compared to the MI model. (aku.edu)
  • Rahimtoola suggested that hibernating myocardium is characterized by a state of persistently impaired myocardial and LV function at rest due to reduced coronary blood flow that can be partially or completely restored to normal by improving blood flow or by reducing oxygen demand (see the image below). (medscape.com)
  • Clinically, discerning the etiology of depressed myocardial contractile function is difficult, whether due to stunned myocardium, silent ischemia, or hibernating myocardium. (medscape.com)
  • Last year, Dharmakumar and Kumar observed that damage to the heart from MI was not only a result of ischemia caused by a blocked artery, but also a result of bleeding in the myocardium after the artery had been opened. (medscape.com)
  • Monophosphoryl lipid A attenuates myocardial stunning in dogs: role of ATP-sensitive potassium channels. (doximity.com)
  • The aim of the study is to investigate the effects of curcumin in attenuates myocardial ischemia and reperfusion-induced proinflammatory response through activation of the Nrf-2/HO-1 signaling pathway. (edu.iq)
  • Inconclusion, this study demonstrates that curcumin attenuates myocardial IRI by inhibiting proinflammatory cytokines through a mechanism that may be related to activation of the Nrf-2/HO-1 signaling pathway. (edu.iq)
  • Thirty Wistar rats were selected and divided into three groups (n = 10): acute ischemia-reperfusion (I/R) group, acute ischemia-reperfusion and treated with atorvastatin group and sham-operated group. (ac.ir)
  • To understand the role of various inflammatory pathways in sepsis and SIRS using mouse models of Caecal Ligation and Puncture (CLP), Lipopolysaccharide (LPS), and acute lung injury mouse models. (edu.au)
  • Treatment of myocardial ischemia, heart failure, and electrolyte disturbances are all justified by the results of multiple acute MI and congestive heart failure randomized trials. (medscape.com)
  • In lpr mice, a naturally occurring mutant deficient in Fas, there is marked reduction in infarct size and abundance of apoptotic cardiac myocytes following ischemia and reperfusion that also signifies the importance of Fas pathway in ischemia-reperfusion injury [ 5 ]. (ac.ir)
  • Effects of three types of bariatric interventions on myocardial infarct size and vascular function in rats with type 2 diabetes mellitus. (almazovcentre.ru)
  • Interrupting reperfusion as a stroke therapy: ischemic postconditioning reduces infarct size after focal ischemia in rats. (ac.ir)
  • We reported that there is infarct expansion after reperfusion, so once you open up the vessel, the heart attack actually gets larger. (medscape.com)
  • The findings of the present study indicated that inhibition of miR‑132 may ameliorate myocardial I/R injury by inhibiting oxidative stress and pyroptosis through activation of PGC‑1α/Nrf2 signalling by targeting SIRT1. (spandidos-publications.com)
  • Meng X, Zhang L, Han B and Zhang Z: PHLDA3 inhibition protects against myocardial ischemia/reperfusion injury by alleviating oxidative stress and inflammatory response via the Akt/Nrf2 axis. (spandidos-publications.com)
  • Rationale: Both cardiomyocyte-restricted proteasome functional enhancement and pharmacological proteasome inhibition (PSMI) were shown to attenuate myocardial ischemia/reperfusion (I/R) injury. (elsevierpure.com)
  • Inhibition of myocardial injury by ischemic postconditioning during reperfusion: comparison with ischemic preconditioning. (ac.ir)
  • 16. Wang Q, Zhang X, Ding Q, Hu B, Xie Y, Li X, Yang Q, Xiong L. Limb Remote Postconditioning Alleviates Cerebral Reperfusion Injury Through Reactive Oxygen Species-Mediated Inhibition of Delta Protein Kinase C in Rats. (ac.ir)
  • The in vitro I/R model was established by the hypoxia/reoxygenation method using H9C2 cells. (spandidos-publications.com)
  • There are still many unknown aspects of MIRI's key molecular mechanisms that merit further study through both in vivo and in vitro MIRI models to discover novel functional molecular targets and identify associated cardioprotective mechanisms, which is important for improving the current treatment of AMI and MIRI. (hindawi.com)
  • Neonatal rat cardiomyocytes were also used to evaluate the protective effect of GRh2 on hypoxia/reoxygenation (H/R)‑induced myocardial injury in vitro. (spandidos-publications.com)
  • To investigate the therapeutic efficacy, pharmacokinetics, and toxicity profile of novel drug treatments using the Experimental Autoimmune Encephalomyelitis (EAE) mouse model, Cuprizone mouse model, and in-vitro models. (edu.au)
  • he also performed research using an in vitro heart model to study ischemia-reperfusion induced myocardial injury and oxidative stress. (healthsnap.io)
  • Bone marrow mesenchymal stem cells (BMSCs) have been reported to attenuate myocardial I/R injury via their paracrine effects, which can be enhanced by hypoxic preconditioning. (researchsquare.com)
  • Recent evidence obtained in mouse models shows its essential role regulating blood cell function through various mechanisms that include pseudohypoxia responses by hypoxia-inducible factor-1α activation, post-translational modifications like succinylation, and communication mediated by succinate receptor 1. (haematologica.org)
  • 18. Wang CX, Yang T, Shuaib A. An improved version of embolic model of brain ischemic injury in the rat. (ac.ir)
  • 20. Zhao H. The protective effect of ischemic postconditioning against ischemic injury: from the heart to the brain. (ac.ir)
  • The ischemic injury underlying these illnesses is complex, involving intricate interplays among many biological functions including energy metabolism, vascular regulation, hemodynamics, oxidative stress, inflammation, platelet activation, and tissue repair that take place in a context- and time-dependent manner. (cdc.gov)
  • Endogenous cardioprotective mechanisms against I/R are impaired in hyperlipidemic and hyperglycemic in vivo animal models. (nih.gov)
  • The present study aimed to investigate the roles of miR‑132 in myocardial ischaemia/reperfusion (I/R) injury and the underlying mechanisms. (spandidos-publications.com)
  • However, despite numerous studies on myocardial I/R injury, deeper insight into the underlying mechanisms of myocardial I/R injury is needed. (spandidos-publications.com)
  • However, few studies have focused on the role of miR-132 in myocardial I/R injury and the underlying mechanisms. (spandidos-publications.com)
  • While effective early reperfusion of the criminal coronary artery after a confirmed AMI is the typical treatment at present, collateral myocardial ischemia-reperfusion injury (MIRI) and pertinent cardioprotection are still challenging to address and have inadequately understood mechanisms. (hindawi.com)
  • Conceptual diagram of the development and unknown mechanisms of myocardial ischemia-reperfusion injury. (hindawi.com)
  • Focus areas: mechanisms of myocardial protection against ischemia-reperfusion injury, development of targeted drug delivery using nanocarriers. (almazovcentre.ru)
  • The key mechanisms underlying myocardial I/R injury include increased intracellular calcium concentration, sudden generation of reactive oxygen species (ROS) and inflammatory cytokines, adenosine triphosphate (ATP) depletion, and development of metabolic acidosis. (researchsquare.com)
  • Delayed postconditionig initiates additive mechanism necessary for survival of selectively vulnerable neurons after transient ischemia in rat brain. (ac.ir)
  • The objectives of this study were to 1) determine the extent to which ascorbate or catechin alone at levels which could be in blood after dietary supplementation, can protect myocardial tissue in the reperfusion phase of I/R injury, and 2) evaluate the possible cooperative or synergistic protective effect of ascorbate and catechin when given together. (usask.ca)
  • During myocardial ischemia (lack of blood flow to the muscle tissue of the heart, commonly referred to as a "heart attack"), blood flow is interrupted because of damage to one or more of the coronary blood vessels that irrigate the heart. (prohealth.com)
  • In many cases, damage to heart tissue by reperfusion injury is greater than the damage done by the interruption of blood flow. (prohealth.com)
  • but reperfusion may introduce additional harm to the tissue through a process known as ischemia/reperfusion injury. (cdc.gov)
  • However, harmful stimuli (such as ischemia-reperfusion, oxidative stress, and toxic chemicals) can change the direction and efficiency of intercellular mitochondrial transfer. (frontiersin.org)
  • The authors carried out tests on an animal model to investigate the individual and combined effects of melatonin and NMN on myocardial function, mitochondrial activity, and oxidative stress status following ischemia/reperfusion injury in aged rat hearts. (prohealth.com)
  • The concomitant presence of myocardial necrosis with myocardial ischemia, stunning, or hibernation may complicate appraisal of left ventricular (LV) function and patient management. (medscape.com)
  • Several imaging modalities have been proposed for accurate assessment of myocardial necrosis, viability, stunning, and hibernation, with mixed results. (medscape.com)
  • Aborted MI (no or minimal myocardial necrosis). (medscape.com)
  • Hydrogen gas can reduce ROS and alleviate cerebral, myocardial, and hepatic ischemia/reperfusion injuries. (molecularhydrogenstudies.com)
  • 0.0417dl · g -1, Cp=0.2663 cal/(g · °C). The hepatoprotective effect of ACN2a was evaluated using a mouse model of hepatic injury that was induced by Propionibacterium acnes (P. acnes) and lipopolysaccharide (LPS). (simpsonbiotech-usa.com)
  • Rats were randomly assigned into sham, model, experimental and control groups. (ijpsonline.com)
  • Therefore, our aim was to develop a medium throughput comorbidity cell-based test system of myocardial I/R injury, hypercholesterolemia and hyperglycemia that mimics comorbidity conditions. (nih.gov)
  • Methods and Results: Myocardial I/R were modeled by ligation (30 minutes) and subsequent release of the left anterior descending artery in mice overexpressing GFPdgn, a validated surrogate proteasome substrate. (elsevierpure.com)
  • The myocardial I/R model was established using C57BL/J6 mice. (spandidos-publications.com)
  • With these webinar opportunities, Cyagen's expert team will comprehensively explain the cutting-edge technology, academic hotspots, and application limitations of animal models - such as genetically modified, humanized, and immunodeficient mice - from various perspectives, as we aim to exchange and share valuable experiences with you and your team. (cyagen.com)
  • The collected exosomes or MSCs were injected intravenously into liver injury mice that had been prepared by the intravenous con-A injection. (biomedcentral.com)
  • It has been shown that the Fas pathway is functional in cardiac myocytes and plays a critical role in myocardial death due to ischemia-reperfusion in vivo [ 4 ]. (ac.ir)
  • The preclinical work focuses on animal models of myocardial ischemia-reperfusion injury, which is an experimental model for STEMI, as well as ex-vivo models of myocardial ischemia. (gu.se)
  • An intravital model for imaging the adult and aged IR-injured beating heart in real time in vivo was used to demonstrate heightened basal and injury-induced neutrophil recruitment, and poorer blood flow, in the aged coronary microcirculation when compared with adult hearts. (jci.org)
  • Ischaemia-reperfusion (I/R) injury is the most important and common cause of myocardial damage and subsequent heart failure worldwide ( 1 , 2 ). (spandidos-publications.com)
  • In addition, it has been shown that atorvastatin can protect the isolated mouse heart against reperfusion-induced injury [ 6 ]. (ac.ir)
  • We reviewed a decade of data from all patients with coronary heart disease enrolled in a single CR center (University of Michigan) to identify the prevalence of low-risk factors, which may inform on consideration for participation in alternative models of CR. (journaltocs.ac.uk)
  • In this observational study, we provide a first paradigm of identifying factors among coronary heart disease patients that may be considered low-risk and likely high-gain for participation in alternative models of CR. (journaltocs.ac.uk)
  • 2007 - Head of Research Laboratory of Myocardial Metabolism, Almazov Federal Heart, Blood and Endocrinology Centre (Almazov National Medical Research Centre). (almazovcentre.ru)
  • Interleukin-36 (IL-36), a newly discovered proinflammatory member of the IL-1 superfamily, may mediate this injury, but its role in the injured heart is currently not known. (jci.org)
  • Therefore, attenuating myocardial I/R injury during the heart transplant procedure would have a favorable impact on improving short- and long-term graft function and recipient's survival(6). (researchsquare.com)
  • Most myocardial infarctions, commonly known as heart attacks, happen in people once they get older, and aging makes it more difficult to recover from this type of injury. (prohealth.com)
  • What Happens During a Heart Attack and Reperfusion Injury? (prohealth.com)
  • Reperfusion injury increases the damage done after events such as heart attacks. (prohealth.com)
  • In pathological conditions, damaged cells transfer dysfunctional mitochondria toward recipient cells to ask for help and take up exogenous functional mitochondria to alleviate injury. (frontiersin.org)
  • Five asthma outcomes-two quality and three morbidity measures-were modeled using generalized estimating equations with a logit link function. (cdc.gov)
  • Ischemic postconditioning may not influence early brain injury induced by focal cerebral ischemia/reperfusion in rats. (ac.ir)
  • 14. Bederson JB, Pitts LH, Tsuji M, Nishimura MC, Davis RL, Bartkowski H. Rat middle cerebral artery occlusion: evaluation of the model and development of a neurologic examination. (ac.ir)
  • 2. Ren C, Yan Z, Wei D, Gao X, Chen X, Zhao H. Limb remote ischemic postconditioning protects against focal ischemia in rats. (ac.ir)
  • 4. Ren C, Gao X, Niu G, Yan Z, Chen X, Zhao H. Delayed postconditioning protects against focal ischemic brain injury in rats. (ac.ir)
  • In conclusion, the present study confirmed that GRh2 could reduce oxidative stress and inflammation in cardiomyocytes after reperfusion, and its mechanism of action may be related to its regulation of the Nrf2/HO‑1/NLRP3 signalling pathway. (spandidos-publications.com)
  • Sun W, Wang Z, Sun M, Huang W and Wang Y and Wang Y: Aloin antagonizes stimulated ischemia/reperfusion-induced damage and inflammatory response in cardiomyocytes by activating the Nrf2/HO-1 defense pathway. (spandidos-publications.com)
  • Numerous apoptotic cardiomyocytes were found in ischemic fields in ischemia-reperfusion groups and werent observed in the sham-operated group. (ac.ir)
  • miR‑132 was significantly upregulated and SIRT1 was markedly downregulated in I/R myocardial tissues. (spandidos-publications.com)
  • Fas expression was significantly higher in the ischemia-reperfusion group as compared to sham-operated group, but was decreased significantly in atorvastatin treated group as compared with I/R group. (ac.ir)
  • At 24 hours of reperfusion, myocardial proteasome activities were significantly lower whereas total ubiquitin conjugates and GFPdgn protein levels were markedly higher in all regions of the I/R hearts than the sham controls, indicative of proteasome functional insufficiency. (elsevierpure.com)
  • However, the necrotic area expressed as a percentage of the myocardial area at risk was significantly lower in the 25 and 50 mmol/kg/hr NaNO2-treated cats. (aspetjournals.org)
  • The resulted data showed that curcumin alleviates myocardial inflammatory responses and oxidative stress during myocardial IRI. (edu.iq)
  • When blood flow is re-established (reperfusion), a series of inflammatory responses take place because of the damage sustained by the tissues affected by the previous lack of blood. (prohealth.com)
  • Over the past three decades, clinical and pharmacological studies have accumulated a body of evidence that not only demonstrated these therapeutic effects, but also provided significant insights into the pharmacokinetic behavior, therapeutic profile, and mode of action of scutellarin in humans and animal models. (cdc.gov)
  • Here we review the current literature on scutellarin to provide a comprehensive understanding of the pharmacological activity, mechanism of action, toxicity, and therapeutic potential of scutellarin for the treatment of ischemia, diabetic complications, and other chronic diseases. (cdc.gov)
  • Systolic wall thickening after coronary artery occlusion and subsequent reperfusion in normal and ischemic zones. (medscape.com)
  • Regional myocardial function and electrophysiological alteration after coronary artery occlusion. (medscape.com)
  • It has been reported that SIRT1/peroxisome proliferator-activated receptor gamma coactivator (PGC)-1α/nuclear factor erythroid-2-related factor 2 (Nrf2) signalling can mediate oxidative stress, which plays an important role in myocardial I/R injury ( 14 , 15 ). (spandidos-publications.com)
  • Until today the activity of such substances had to be tested in animal models because of complex interactions between endothelial cells, coagulation and innate immunity. (forschung3r.ch)
  • One strategy that has produced successful results in animal models is the restoration of cellular NAD+ by supplementation with the NAD+ precursor NMN (nicotinamide mononucleotide) (3). (prohealth.com)
  • This study aimed to evaluate the effect of mesenchymal stem cell (MSC)-derived exosomes on an immune-induced liver injury model. (biomedcentral.com)
  • This research is undertaken to evaluate the effect of MSC-derived exosome on concanavalin-A (con-A)-induced liver injury. (biomedcentral.com)
  • Suppression of con-A-induced liver injury by injection of exosomes was observed as same extent as MSC. (biomedcentral.com)
  • In this study, we investigated the suppressive effect of exosomes on an immune-induced liver injury model. (biomedcentral.com)
  • The liver injury was induced by injection of concanavalin A (con-A), a lectin derived from jack beans. (biomedcentral.com)
  • This type of liver injury is mediated through activation of the adaptive immune system including natural killer and Kupffer cells, which is employed as a method to evaluate the induction liver tolerance [ 19 - 21 ]. (biomedcentral.com)
  • The suppressive effects of MSC-derived exosomes and the MSCs in this injury model were evaluated by the level of plasma alanine aminotransferase (ALT), histopathological examinations, the messenger RNA (mRNA) expression of pro- and anti-inflammatory cytokines, and the population alteration of regulatory T cells (Treg) among non-parenchymal liver cells (NPCs). (biomedcentral.com)
  • Model of Chronic Thromboembolic Pulmonary Hypertension in Rats Caused by Repeated Intravenous Administration of Partially Biodegradable Sodium Alginate Microspheres. (almazovcentre.ru)
  • In the present study, authors aim to investigate whether hydrogen-rich saline can reduce neuropathic pain in a rat model of chronic constriction injury (CCI). (molecularhydrogenstudies.com)
  • Myocardial reperfusion is the restoration of coronary blood flow after a period of coronary occlusion. (aku.edu)
  • 11. Dinapoli VA, Rosen CL, Nagamine T, Crocco T. Selective MCA occlusion: a precise embolic stroke model. (ac.ir)
  • Acidified NaNO2 (12.5-50 mmol/kg/hr) was infused i.v., starting 30 min postocclusion followed by reperfusion 1 hr later, in cats subjected to MI by occlusion of the left anterior descending coronary artery. (aspetjournals.org)
  • Heyndrickx et al observed that after 5 minutes of occlusion in the left anterior descending coronary artery, surface electrocardiogram (ECG) findings and regional contraction (with reperfusion) rapidly normalized. (medscape.com)
  • The use of comorbidity models is crucial in cardioprotective drug development. (nih.gov)
  • Commercial kits were used to measure the levels of serum myocardial enzymes and inflammatory factors. (spandidos-publications.com)
  • Apparent histologic injury and elevated levels of serum myocardial enzymes and inflammatory factors were observed in the myocardial I/R model. (spandidos-publications.com)
  • The GRh2 pre‑treatment reduced the I/R‑ or H/R‑induced release of myocardial enzymes and the production of IL‑1β, IL‑18 and TNF‑α. (spandidos-publications.com)
  • In conclusion, this study showed strong protection by ascorbate, which could be used in clinically relevant situations, and is the first to report the protection by catechin at this dose under conditions of myocardial ischemia-reperfusion injury. (usask.ca)
  • Conclusion: Salvia miltiorrhiza injection maintains normal function of blood platelets and ameliorates myocardial ischemia-reperfusion injury by decreasing expression of PECAM-1. (archive.org)
  • Purpose: To investigate the effect of Salvia miltiorrhiza injection on myocardial ischemia-reperfusion injury and PECAM-1 related pathways. (archive.org)
  • Recovery of myocardial contractile function after spontaneous restoration of flow may be protracted similarly after angioplasty or revascularization surgery. (medscape.com)
  • Additionally, gene-edited animal models are widely adopted by drug R&D companies, scientific research institutions, and laboratories worldwide in analyzing the function of disease-related genes, studying signaling pathways, identifying drug targets, screening new drugs, and more. (cyagen.com)
  • Evidence for the involvement of the ATP-sensitive potassium channel in a novel model of hypoxic preconditioning in dogs. (doximity.com)
  • To evaluate the effects of dexmedetomidine on myocardial ischemia-reperfusion injury in rats and its anti-apoptotic role, as well as the mechanism by which it regulates Janus kinase 2/signal transducers and activators of transcription 3 signal. (ijpsonline.com)
  • Animal modeling has a played a prominent role in traditional scientific research for hundreds of years, and more recently, inbred strains have been developed to support genetically modified models for applications in biomedical and health research. (cyagen.com)
  • Previous studies have shown that ischemia/reperfusion (I/R) injury acts as a significant role in PGD(4), contributing to adverse short- and long-term clinical outcomes in the recipients. (researchsquare.com)
  • In cases of less severe ischemia, some myocytes remain viable but have depressed contractile function. (medscape.com)
  • When ischemia is prolonged, myocytes have depressed contractile function but remain viable. (medscape.com)
  • The ensuing vasoplegia, coagulopathy, and depressed myocardial function present numerous challenges during the weaning process, as well as during the following hours in the intensive care unit (ICU). (medscape.com)