• these socalled pleiotropic properties include anti-inflammatory effects, plaque stabilization, improved endothelial function and inhibition of vascular smooth muscle cell proliferation. (ac.ir)
  • Thus, inhibition of oxidative stress and myocardial apoptosis is beneficial in the treatment of myocardial I/R injury. (spandidos-publications.com)
  • Inhibition of Sema4D attenuates pressure overload-induced pathological myocardial hypertrophy via the MAPK/NF-\\xce\\xbaB/NLRP3 pathways. (brain-knowledge-engine.org)
  • Dexmedetomidine abates myocardial ischemia reperfusion injury through inhibition of pyroptosis via regulation of miR-665/MEF2D/Nrf2 axis. (brain-knowledge-engine.org)
  • The cardioprotective effect of CLU4A inhibition was detected by monitoring the cell viability, cell apoptosis, and LDH activity in vitro and in vivo , and examining the infarct size and cardiac function in vivo . (engreen.com.cn)
  • Inhibition of CLU4A exhibited a cardioprotective role by an ERK-dependent pathway. (engreen.com.cn)
  • The effects of acidified sodium nitrite (NaNO2) which releases nitric oxide, a substance which is thought to be indistinguishable from endothelium-derived relaxing factor, were investigated in a 6-h model of myocardial ischemia (MI) with reperfusion in open-chest, anesthetized cats. (aspetjournals.org)
  • Wogonin could suppress apoptosis in rats experienced myocardial I/R [ 25 ]. (hindawi.com)
  • Together, the results of the current study suggest that the protective effect of vitexin reduces sevoflurane‑induced neuronal apoptosis through HIF‑1α‑, VEGF‑ and p38‑associated signaling pathways in newborn rats. (spandidos-publications.com)
  • 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)
  • 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)
  • This study aimed to evaluate the effects of TQ on spatial memory and hippocampal long-term potentiation (LTP) in rats with thioacetamide (TAA)-induced liver injury and hepatic encephalopathy. (magiran.com)
  • Acomparative study on the beneficial effects of garlic ( Allium sativum Linn), amla ( Emblica Officinalis Gaertn) and onion ( Allium cepa Linn) on the hyperlipidemia induced by butter fat and beef fat in rats. (ac.ir)
  • We investigated the effects of estrogen on global myocardial ischemia-reperfusion injury in rats that were ovariectomized (Ovx), sham-operated, or ovariectomized and then given 17β-estradiol (E 2 β) supplementation (Ovx+E 2 β). (illinois.edu)
  • Our results indicate that estrogen plays a cardioprotective role in global myocardial ischemia-reperfusion injury in female rats. (illinois.edu)
  • we found that the conditioned medium effectively promoted the recovery of sensory and motor functions in rats with spinal cord injury, decreased expression of the microglial pyroptosis markers nlrp3 , gsdmd , caspase-1, and interleukin-1\xce\xb2, promoted axonal and myelin regeneration, and inhibited the formation of glial scars. (brain-knowledge-engine.org)
  • Effect of Gualou Xiebai Decoction on pulmonary fibrosis in rats based on pyroptosis pathway]. (brain-knowledge-engine.org)
  • In this study, we investigated that if CDP-choline has protective effects against long-term myocardial ischemia-reperfursion injury in rats.Long term ischemia-reperfusion was produced in anaesthetized rats by ligature of the left main coronary artery for 30 minutes followed by reperfusion period for the next 180 minutes. (uludag.edu.tr)
  • We aimed to investigate the effect of PLCA on hypoxia/reoxygenation (H/R) in neonatal rat ventricular myocytes (NRVM) and on myocardial I/R in rats. (biomedcentral.com)
  • The accumulation of cardiac lactate was attenuated by PLCA during myocardial I/R, and infarct size was smaller in rats treated with PLCA (1 mg/kg) than in those treated with caffeic acid (1 mg/kg). (biomedcentral.com)
  • Ischemia was induced in male (M-Isch) and female (F-Isch) rats with sc. (biomedcentral.com)
  • This study investigated the effect of the trans-resveratrol supplementation on the cardiac oxidative stress in rats exposed to cigarette smoke. (bvsalud.org)
  • Our findings evidenced the cardioprotective effect of trans- resveratrol in rats exposed to cigarette smoke. (bvsalud.org)
  • H2S decreases injury through many different effects such a decrease in oxidative stress, maintenance of mitochondrial function, and increased eNOS (endothelial nitric oxide synthase) activation. (wikipedia.org)
  • Evidence that mitochondrial respiration is a source of potentially toxic oxygen free radicals in intact rabbit hearts subjected to ischemia and reflow. (ac.ir)
  • 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)
  • 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)
  • Intracellular mechanisms underlying this so-called reperfusion injury presumably include increased levels of reactive oxygen species, Ca 2+ overload, rapid restoration of physiologic pH, and inflammatory processes resulting in opening of the mitochondrial permeability transition pore (mPTP). (silverchair.com)
  • Mitochondrial dysfunction and oxidative damage are major contributors to myocardial apoptosis during I/R injury. (wustl.edu)
  • We hypothesize that SAHA protects the myocardium by maintaining mitochondrial homeostasis and reducing reactive oxygen species (ROS) production during I/R injury. (wustl.edu)
  • 50% loss of mtDNA content in the border zones of mouse hearts, but SAHA pretreatment and reperfusion treatment alone reverted mtDNA content and mitochondrial mass to control levels. (wustl.edu)
  • However, loss-of-function of ATG7 in cardiomyocytes or mouse myocardium abolished the protective effects of SAHA on ROS levels, mitochondrial membrane potential, mtDNA levels, and mitochondrial mass. (wustl.edu)
  • Lastly, PGC-1α gene expression was induced by SAHA in NRVMs and mouse heart subjected to I/R, and loss of PGC-1α abrogated SAHA's mitochondrial protective effects in cardiomyocytes. (wustl.edu)
  • Conclusions: SAHA prevents I/R induced-mitochondrial dysfunction and loss, and reduces myocardial ROS production when given before or after the ischemia. (wustl.edu)
  • The protective effects of SAHA on mitochondria are dependent on autophagy and PGC-1α-mediated mitochondrial biogenesis. (wustl.edu)
  • Previous hypothesis-driven experiments have highlighted the role of sex hormones on distinct inflammatory responses, mitochondrial proteins, extracellular remodeling and estrogen-mediated cardioprotective signaling pathways related to post-ischemic recovery, which were associated with better cardiac functional outcomes in females. (biomedcentral.com)
  • Vascular endothelial cell (EC)-derived factors play an important role in endothelial-cardiomyocyte crosstalk and could save cardiomyocytes (CMs) from injury. (mdpi.com)
  • Res effectively suppress the cardiomyocytes hypertrophy and apoptosis induced by ISO, characterized by the reduction of the myocardial cell surface area, the ANP gene expression, the LDH and MDA leakage amount and the rate of cell apoptosis, while decrease of the protein expression of GRP78, GRP94 and CHOP, and reverse the expression of Bcl-2 and Bax. (karger.com)
  • leaves alleviate hypoxia/reoxygenation (H/R) injury in H9c2 cardiomyocytes and to explore potential mechanisms. (hindawi.com)
  • Numerous apoptotic cardiomyocytes were found in ischemic fields in ischemia-reperfusion groups and werent observed in the sham-operated group. (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)
  • In conclusion, the present study demonstrated that SA inhibits the apoptosis of H9c2 cardiomyocytes following H/R injury via reduced activation of the p38MAPK and JNK signaling pathways. (spandidos-publications.com)
  • The results demonstrated that SA inhibited apoptosis signaling in H9c2 cardiomyocytes via downregulation of p38 mitogen-activated protein kinase (p38MAPK) and c-Jun N-terminal kinase (JNK) signaling pathways following hypoxia/reoxygenation (H/R) injury. (spandidos-publications.com)
  • Methods: Mouse and cultured cardiomyocytes (neonatal rat ventricular myocytes and human embryonic stem cell-derived cardiomyocytes) I/R models were used to investigate the effects of SAHA on mitochondria. (wustl.edu)
  • Cardiomyocytes were isolated and subjected to 6 h hypoxia followed by 18 h reperfusion. (biomedcentral.com)
  • Z-Ligustilide (LIG), the primary lipophilic component of the Chinese traditional medicine Radix Angelica Sinensis, has been shown to reduce ischemic brain injury via anti-apoptotic pathways. (alexbotsaris.com.br)
  • The molecular mechanism was further determined by examining the effects of PD98059, a specific inhibitor of the ERK signaling pathways in H9C2 cells with hypoxia/reoxygenation treatment. (engreen.com.cn)
  • Identifying the molecules and cellular signal pathways implicated in these processes will be crucial for creating effective tissue-preserving treatments during or after reperfusion. (unab.cl)
  • This review provides a current summary of the principal molecules, pathways, and mechanisms underlying cardiomyocyte and cardiac fibroblast crosstalk during ischemia/reperfusion injury. (unab.cl)
  • Adaptation to chronic hypoxia increases myocardial resistance to acute ischemia/reperfusion (I/R) injury, similarly to application of exogenous erythropoietin (EPO). (nusl.cz)
  • Nevertheless, it is not known if EPO induced by chronic hypoxia plays a role in its cardioprotective mechanism. (nusl.cz)
  • The aim of this study was to find out if protective effect of exogenous EPO adds up to protection offered by chronic hypoxia. (nusl.cz)
  • The results indicate that exogenous EPO employs the same cardioprotective mechanisms as adaptation to chronic intermittent hypoxia. (nusl.cz)
  • This article reviews the anti-inflammatory relative and anti-infectious effects of Evodia rutaecarpa and its major bioactive components and the involvement of the nitric oxide synthases, cyclooxygenase, NADPH oxidase, nuclear factor kappa B, hypoxia-inducible factor 1 alpha, reactive oxygen species, prostaglandins, tumor necrosis factor, LIGHT, amyloid protein and orexigenic neuropeptides. (biomedcentral.com)
  • CLU4A expression was measured after myocardial ischemia/reperfusion in mice and in H9C2 cells with hypoxia/reoxygenation treatment by q-PCR and western blotting. (engreen.com.cn)
  • Additionally, machine reperfusion induces the production of ROS, which results in I/R injury to the heart. (gotomydoctor.com)
  • The uncoupling of glycolysis and glucose oxidation induces lactate accumulation during myocardial ischemia/reperfusion (I/R) injury. (biomedcentral.com)
  • The heart was preperfused with Krebs-Henseleit (K-H) solution containing T. polium extract for 20 min before 20 min global ischemia, and then the reperfusion with K-H bicarbonate buffer was conducted for 40 min. (ac.ir)
  • H2S is a cardioprotective agent that has antioxidant, anti-inflammatory, and anti-apoptotic effects. (wikipedia.org)
  • With the same phenolic hydroxyl substitutions, in vitro experiments demonstrated that both low concentrations of aglycone of AG (apigenin) and high concentrations of flavanone naringenin can produce the same anti-inflammatory effect, and the inhibitory effect of the flavonol Kaempferol on TNF-α was around 20% less than that of apigenin at the same concentration. (frontiersin.org)
  • Previous studies have demonstrated that Vitexin possesses antihypertensive, anti‑inflammatory and potential anticancer effects. (spandidos-publications.com)
  • In recent years, it has been reported that vitexin has anti-inflammatory effect ( 10 ). (spandidos-publications.com)
  • Due to its well-documented anti-inflammatory properties and antioxidant effects, melatonin has been widely studied for use as a cardioprotectant. (prohealth.com)
  • This article reviews the anti-inflammatory relative and anti-infectious effects of Evodia rutaecarpa ( Wuzhuyu ) and its major bioactive components such as dehydroevodiamine (DeHE), evodiamine (Evo) and rutaecarpine (Rut). (biomedcentral.com)
  • Mechanisms of anti-inflammatory relative effects of Evodia rutaecarpa and its bioactive components are summarized in Additional file 1 . (biomedcentral.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)
  • Aims: The FDA-approved histone deacetylase (HDAC) inhibitor, suberoylanilide hydroxamic acid (SAHA, Vorinostat) has been shown to induce cardiomyocyte autophagy and blunt ischemia/reperfusion (I/R) injury when administered at the time of reperfusion. (wustl.edu)
  • In order to fully understand the mechanisms of I/R injury and to find novel therapeutic strategies, further research is stilled urgently needed [ 3 ]. (hindawi.com)
  • The present study aimed to investigate whether the protective effect of vitexin protects against sevoflurane-induced neuronal apoptosis and the underlying mechanisms of this protective effect. (spandidos-publications.com)
  • Ischemic preconditioning, postconditioning, and remote conditioning trigger endogenous cardioprotective mechanisms that render the heart more resistant to lethal ischemic-reperfusion injury. (nih.gov)
  • However, major cardiovascular co-morbidities such as hyperlipidemia, diabetes, and their co-medications interfere with these cardioprotective mechanisms thereby limiting the efficacy of cardioprotective ischemic conditioning maneuvers. (nih.gov)
  • The present study aimed to clarify the cardioprotective effect of SA in myocardial I/R injury in vitro and explore the potential molecular mechanisms. (spandidos-publications.com)
  • The underlying mechanisms behind myocardial I/R injury are associated with a number of factors, including substantial free radical production, intracellular calcium overload, increased inflammation, myocardial necrosis and apoptosis ( 6 ). (spandidos-publications.com)
  • The present study aims to clarify the inhibitory effect of ASP on hepcidin expression as well as the involved mechanisms. (alexbotsaris.com.br)
  • However, the precise mechanisms underlying the cardioprotective activity of SAHA are unknown. (wustl.edu)
  • We investigated the effects of a fibrin-derived peptide Bbeta(15-42) in acute and chronic rodent models of ischemia-reperfusion at three different study centers (Universities of Dusseldorf and Vienna, TNO Biomedical Research). (bris.ac.uk)
  • Reperfusion treatment has a potential risk of worsening tissue damage after ischemia, which can accelerate the deterioration of cardiac function [ 2 ]. (hindawi.com)
  • Thiobarbituric acid reactive substances (TBARS), total thiol groups (−SH), superoxide anion dismutase (SOD), and catalase (CAT) in myocardial tissue were detected to determine the oxidative stress degree. (ac.ir)
  • During events such as heart attacks or strokes, blood flow is interrupted and the tissue that is affected by this lack of blood becomes injured. (prohealth.com)
  • 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)
  • The affected tissue also releases excessive amounts of reactive oxygen species (ROS) that increase damage through oxidative stress. (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)
  • Numerous therapies to protect cardiac tissue from reperfusion-induced injury have been explored, and ample pre-clinical research has attempted to identify drugs or techniques to mitigate cardiac damage. (unab.cl)
  • FFPE tissue slides were scanned and analyzed digitally, while myocardial proteins were quantified by liquid chromatography-tandem mass spectrometry (LC-MS/MS) using isobaric labeling. (biomedcentral.com)
  • This study was undertaken to investigate whether Res can protect the heart suffering from hypertrophy injuries induced by isoproterenol (ISO), and whether the protective effect is mediated by endoplasmic reticulum (ER) stress. (karger.com)
  • In summary, Res treatment effectively suppressed myocardial hypertrophy and apoptosis at least partially via inhibiting ER stress. (karger.com)
  • further research indicated that myocardial hypertrophy induced by sema4d was closely related to the expression of the pyroptosis-related proteins pp65, nlrp3 , caspase-1, asc, gsdmd , il-18 and il-1\xce\xb2. (brain-knowledge-engine.org)
  • Consistently, knockdown of CLU4A reduced the myocardial infarct size and improved cardiac function in vivo . (engreen.com.cn)
  • Ischemia reperfusion injury and cardioprotection by conditioning have been shown to affect global myocardial gene expression profile at the transcript level. (nih.gov)
  • Further understanding and the comprehensive analysis of the cardioprotective gene expression fingerprint in normal, protected, and in comorbid conditions may lead to identification of novel molecular targets for cardioprotection. (nih.gov)
  • However, beta-adrenergic signaling displays a differential role in cardioprotection during reperfusion. (silverchair.com)
  • Esmolol given during the initial 30 min of reperfusion had no effect on infarct size (54 +/- 4%) but blocked desflurane-induced postconditioning (58 +/- 5%), whereas esmolol administered throughout reperfusion reduced infarct size in the absence or presence of desflurane to 42 +/- 6% and 41 +/- 7%, respectively. (silverchair.com)
  • ICI 118,551 and KN-93 did not affect infarct size (62 +/- 4% and 62 +/- 6%, respectively) but abolished desflurane-induced postconditioning (57 +/- 5% and 64 +/- 3%, respectively). (silverchair.com)
  • One such approach is pharmacological postconditioning, in which a cardioprotective agent is administered coincidentally with flow restoration. (justia.com)
  • Postconditioning using N-Ac-GLP-1(7-34)amide N-terminally blocked and C-terminally truncated results in a limitation of ischemia-reperfusion injury in an isolated rat heart. (justia.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)
  • abstract = "Many compounds have been shown to prevent reperfusion injury in various animal models, although to date, translation into clinic has revealed several obstacles. (bris.ac.uk)
  • Abstract: The effects of Cordyceps sinensis (CS) and its extracted fractions on steroidogenesis in MA-10 cells were determined. (simpsonbiotech-usa.com)
  • Abstract: The stimulatory effect of Cordyceps sinensis (CS) on MA-10 mouse Leydig tumor cell steroidogenesis was previously demonstrated in our laboratory. (simpsonbiotech-usa.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)
  • Apelin protects heart against ischemia/reperfusion injury in rat. (ac.ir)
  • Extract from Clerodendron colebrookianum Walp protects rat heart against oxidative stress induced by ischemic-reperfusion injury (IRI). (ac.ir)
  • Moreover, it was observed that, PGRN protects the heart against ischemia-reperfusion injury. (biomedcentral.com)
  • Thus, acidified NaNO2 exerts a significant protective action during ischemia and reperfusion injury, which suggests that endothelium-derived relaxing factor has a cardioprotective effect in MI. (aspetjournals.org)
  • Although, CDP-choline treatment did not significantly alter the blood levels of any parameter (ADMA, M30, M65, homocysteine, serum lipid profile).Results of this study show that CDP-choline exerts cardioprotective effects in long term myocardial ischemia-reperfusion injury. (uludag.edu.tr)
  • Metformin also exerts a protective effect to both vascular and neural-networks. (jaycampbell.com)
  • Upregulation of HIF-1 expression may play a neuroprotective role in animal models of focal cerebral ischemia ( 6 ). (spandidos-publications.com)
  • The current study aimed to investigate the neuroprotective effects of P. minus ethanolic extract (PMEE) on H2O2-induced neurotoxicity in SH-SY5Y cells. (bvsalud.org)
  • The results indicate that PMEE has neuroprotective effects on SH-SY5Y neuroblastoma cells in vitro. (bvsalud.org)
  • The myocardial apoptosis and inflammation have been recognized as features of I/R injury. (hindawi.com)
  • Inflammation is a protective physiological response of an organism to chemical, physical, infectious agents, environmental toxins, ischemia or an antigen-antibody interaction. (biomedcentral.com)
  • The protective effects of TFs resulted in higher expression of miR-21 in H/R-induced H9c2 cells than that of controls, which in turn upregulated Akt signaling activity via suppressing the expression of PTEN together with decreasing the ratio of Bax/Bcl-2, caspase3, and cleaved-caspase3 expression in H/R-induced H9c2 cells. (hindawi.com)
  • To test this hypothesis, we attempted to investigate whether TFs can exert its cardioprotective effect and the effects of TFs on miR-21 in H9c2 cells. (hindawi.com)
  • dex markedly augmented cell viability, while suppressing cell apoptosis and expressions of nlrp3 , cleaved-caspase-1, asc, gsdmd , il-1\xce\xb2, and il-18 in h9c2 cells subjected to h/r injury. (brain-knowledge-engine.org)
  • Cytidine diphosphocholine (CDP-choline) is in use for treatments of stroke and head trauma in Japan and several European countries for many years because of its protective effect against cerebral injury. (uludag.edu.tr)
  • Ischaemic reperfusion injury (IRI) after tourniquet release during total knee arthroplasty (TKR) is related to postoperative cerebral complications. (medsci.org)
  • Thus, we evaluated the effect of RIPC on regional cerebral oxygenation after tourniquet release during TKR. (medsci.org)
  • Research suggests that Guava has cardioprotective effects against myocardial ischemia-reperfusion injury in isolated rat hearts, primarily through their radical-scavenging actions. (uconn.edu)
  • Apart from endothelium dependence, alpha 1-adrenoceptor blockade, K + channel activation and Ca 2+ channel blockade were also involved in the vasorelaxant effect of DeHE [ 7 ]. (biomedcentral.com)
  • Coupled with influx of extracellular calcium, Rut produced the endothelium-dependent vasorelaxant effect by activation of endothelium NOS and release of NO without pertussis toxin-sensitive Gi protein and other G proteins or phospholipase C activation being involved [ 8 ]. (biomedcentral.com)
  • Tourniquet release during the late period of TKR can induce ischaemic-reperfusion injury, eliciting the activation of neutrophils, circulating pro-inflammatory cytokines, and reactive oxygen species [ 2 , 3 ]. (medsci.org)
  • This effect is attributed to increased reactive oxygen species (ROS) within cancer cells, increased the number of cells that arrest in the G2 phase of mitosis, and promote an increase in caspase-3 activity. (wikipedia.org)
  • End of the experiments we collected blood samples for the measurement of endothelial dysfunction parameter asymmetric dimethylarginine (ADMA), apoptosis parameters M30 and M65, cardiac risk factors homocysteine and serum lipid profile.CDP-choline treatment significantly attenuated the size of infarct area induced by long term ischemia-reperfusion versus saline group. (uludag.edu.tr)
  • Monophosphoryl lipid A attenuates myocardial stunning in dogs: role of ATP-sensitive potassium channels. (doximity.com)
  • Effects of monophosphoryl lipid A on myocardial ischemia/reperfusion injury in dogs. (doximity.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)
  • Conversely, blocking miR-21 expression with miR-21 inhibitor effectively suppressed the protective effects of TFs against H/R-induced injury. (hindawi.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 results indicated that TFs significantly alleviate H/R injury, which include inhibiting apoptosis and enhancing antioxidant capacity. (hindawi.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)
  • Reperfusion injury is a significant threat to myocardial function that arises with the reintroduction of blood flow to the heart following an ischemic episode. (wikipedia.org)
  • The mitochondria has been known to protect the heart from ischemic-reperfusion injury through the opening of the ATP-sensitive K+ channel. (wikipedia.org)
  • In addition, it has been shown that atorvastatin can protect the isolated mouse heart against reperfusion-induced injury [ 6 ]. (ac.ir)
  • Since Teucrium polium has anti-oxidative and cardio-protective properties, the aim of this study was to investigate the effects of this plant on I/R injuries in the isolated rat heart. (ac.ir)
  • Conclusions: Our findings indicated that T. polium could provide protection for heart against the I/R injury which may be related to the improvement of myocardial oxidative stress states. (ac.ir)
  • 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)
  • So, researchers are trying to understand how aging affects the heart and determine what treatments are best suited for heart damage given a person's age. (prohealth.com)
  • A study published by Hosseini and colleagues brings us a step closer to addressing this detrimental disease by testing a pair of compounds that may have protective effects against heart damage in older people. (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)
  • The extent of reperfusion injury is directly proportional to preservation time in cold storage, and research has shown that with static storage methods, heart storage time will not exceed six hours. (gotomydoctor.com)
  • Therefore, we propose to investigate the effect of varying NaHS concentrations on heart cell viability. (gotomydoctor.com)
  • The invention pertains to a polypeptide for the protection against heart ischemia-reperfusion injury. (justia.com)
  • One object of the present invention is to provide a therapy of heart ischemia-reperfusion injury by applying GLP-1 analogues which can be administered as single component and avoiding administration of the drug with a second compound. (justia.com)
  • The present invention is based on the surprising finding that the peptides of the invention have protective cardiovascular effects without simultaneous administration of other compounds, specifically they have protective effects on the heart against ischemia-reperfusion injury. (justia.com)
  • Coronary heart disease is a leading cause of death in the world and therapy to reduce injury is still needed. (biomedcentral.com)
  • With ischemia in coronary heart disease, impairment of the oxygen supply and metabolic disorder both occur [ 2 ]. (biomedcentral.com)
  • Facilitation of glucose utilization contributes to the protective effect of AKT signaling to reduce infarct size and improve myocardial function in a heart subjected to I/R [ 15 ]. (biomedcentral.com)
  • However, most of the studies on RIPC have been conducted only in the heart or kidney models in animals [ 9 , 10 , 12 - 14 ], and few studies have evaluated the beneficial effect of RIPC during TKR. (medsci.org)
  • stopping the heart also markedly decreases myocardial oxygen demand. (msdmanuals.com)
  • Then the aorta is cross-clamped and the heart is stopped by injection of a cardioplegic solution (crystalloid or more commonly blood-based) that also contains substances that help myocardial cells tolerate ischemia and reperfusion. (msdmanuals.com)
  • Despite cardioprotective measures, stopping the heart is not without consequences. (msdmanuals.com)
  • Beneficial effects of octreotide in alcohol-induced neuropathic pain. (ooir.org)
  • Beneficial role of oleuropein in sepsis-induced myocardial injury. (ooir.org)
  • 1. The objective is to evaluate the relationship between concentration of NaHS and its effect on viability by performing a dose-response test in order to evaluate the concentration of NaHS with the most beneficial results to tissues. (gotomydoctor.com)
  • This beneficial effect of N-Ac-GLP-1(7-34)amide was manifested through a diminished diastolic hypercontracture and diminished infarct size. (justia.com)
  • Considering that tourniquet application during TKR is related to ischaemic injury, the organ protective effect of ischaemic preconditioning can have a beneficial role after tourniquet release during TKR. (medsci.org)
  • Reperfusion triggers an inflammatory response and often results in oxidative damage. (wikipedia.org)
  • 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)
  • Meanwhile, the organ protective effect of ischaemic preconditioning could be induced when the episodic ischaemia is at distant tissues or organs, the concept being termed remote ischaemic preconditioning (RIPC) [ 9 ]. (medsci.org)
  • Our study has highlighted sex-specific alterations in systolic and diastolic function shortly after ischemia, and provided a comprehensive look at the underlying proteomic changes and the influence of estrogens and their metabolites. (biomedcentral.com)
  • PLCA at 1 μM and metformin at 30 μM exerted similar effects on the improvement of cell viability and the alleviation of cell apoptosis in NRVM after H/R. PLCA promoted p-AMPK, p-AKT, and GLUT4 upregulation to induce a cardioprotective effect in both cell and animal model. (biomedcentral.com)
  • It was shown that functional Fas system contributes to apoptotic myocardial cell death in response to ischemia/reperfusion injury [ 4 , 5 ]. (ac.ir)
  • Additionally, treatment reduced the number of apoptotic cells in the surrounding brain injury site which accompanied a marked down-regulation of pro-apoptotic proteins, p53 and cleaved caspase-3. (alexbotsaris.com.br)
  • Hypoxic adaptation decreased infarct area to 23,49 ± 2,30%, but additive effect of EPO in hypoxic group was not detected. (nusl.cz)
  • The hearts of the animals were removed and stained with a histologic dye at the end of the reperfusion and risk area/infarct area percent ratio was calculated. (uludag.edu.tr)
  • AG has emerged as a research hotspot in recent years due to its outstanding bioactivities and promising therapeutic effects for numerous diseases. (frontiersin.org)
  • Therapeutic effects of AG against multiple diseases. (frontiersin.org)
  • A therapeutic drug that targets ischemia reperfusion (I/R) injury is needed and has yet to be developed. (biomedcentral.com)
  • 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)
  • Treatment agents (Saline 1 ml/kg, CDP-kolin 100, 250, 500 mg/kg, intravenously) were given in the middle of the ischemia. (uludag.edu.tr)