InfarctionDysfunctionIschemicInhibitionAcuteCoronary arteryLeft ventricularVentricularInfarct sizeMyocardiumOxidativeApoptosis in ratsEndogenousVitroDamage in ratsPretreatmentCerebral ischemiaHypertrophyPathwaysMitochondrial biogenesisSprague-DawleyHypoxiaProtectsExperimentalInjury inducedPathwayCell apoptosisMiceArrhythmiasMethodsIsolated rat heartsLipopolysaccharideLactateSIRT1Cardioprotective effectsMechanismsInhibitsMyocytesInflammationAutophagyCardiac functionSerumSuppressDiabeticNeuroprotectiveSignificantlyHeartConcentrationsProtective effectsTreatmentSenescenceSpinalReductionTissuesTherapeutic1993Effect
Infarction14
- Growth differentiation factor 15 as an integrative biomarker of heart failure in patients with acute myocardial infarction. (escardio.org)
- Progenitor cell therapy in a porcine acute myocardial infarction model induces cardiac hypertrophy, mediated by paracrine secretion of cardiotrophic factors including TGFbeta1. (sciendo.com)
- A quantitative, randomized study evaluating three methods of mesenchymal stem cell delivery following myocardial infarction. (sciendo.com)
- However it causes unwanted side effects, and may induce myocardial infarction [ 4 ]. (walshmedicalmedia.com)
- The cardioprotective effects of Nar are well documented in the healthy state, in myocardial infarction, and in daunorubicin-, doxorubicin-, and high-glucose-induced cardiotoxicity [ 2 , 12 - 17 ]. (hindawi.com)
- Following myocardial infarction (MI), the myocardium is prone to calcium-driven alternans, which typically precedes ventricular tachycardia and fibrillation. (frontiersin.org)
- Cardiovascular diseases (CVDs) encompass all pathologies of the heart or circulatory system, including coronary artery disease (CAD), myocardial infarction (MI), heart failure and peripheral vascular disease. (encyclopedia.pub)
- Atherosclerosis is the main contributor to myocardial infarction. (uni-frankfurt.de)
- In conclusion, apoptosis in advanced plaques seems to be a double edged sword: apoptosis of VSMCs may lead to plaque rupture due to diminished collagen synthesis and following myocardial infarction. (uni-frankfurt.de)
- The study aims to examine the effects of coenzyme Q10, (a bioenergetic antioxidant), on the indexes of left ventricular remodeling, oxidative damage, and angiotensin-converting enzyme (ACE) level after acute myocardial infarction (AMI) with left ventricular dysfunction. (mdpi.com)
- Cell death occurs and finally leads to myocardial infarction. (biomedcentral.com)
- Cell apoptosis occurs, such as by activation of caspase-3 activity, and finally leads to myocardial infarction [ 1 ]. (biomedcentral.com)
- Patients often present with chest pain, have ST-segment elevation on electrocardiogram, and elevated cardiac enzyme levels consistent with a myocardial infarction. (medscape.com)
- Stroke and myocardial infarction are among the most common causes of mortality and disability in the world. (cdc.gov)
Dysfunction8
- Mehta JL, Nichols WW, Donnelly WH, Lawson DL, Thompson LV, ter Riet M, Saldeen TGP: Protection by superoxide dismutase from myocardial dysfunction and attenuation of vasodilator reserve following coronary occlusion and reperfusion in dog. (wikipedia.org)
- Platelets protect against myocardial dysfunction and injury induced by ischemia and reperfusion in isolated rat hearts. (wikipedia.org)
- Post-ischemic stroke-induced myocardial dysfunction is associated with nitro-oxidative stress and sympathetic overactivity. (escardio.org)
- Hypercholesterolemia causes endothelial and myocardial dysfunction, as well as aggravates ischemia/reperfusion (I/R)-induced myocardial injury. (nih.gov)
- Mitochondrial dysfunction and oxidative damage are major contributors to myocardial apoptosis during I/R injury. (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)
- Some authors have proposed a unifying hypothesis stating that in susceptible individuals, notably women, neurohormonal stimulation results in acute myocardial dysfunction, as reflected by the characteristic left ventricular wall-motion abnormality of TCM. (medscape.com)
- These factors affect the way in which the immature heart handles calcium, which, in turn, contributes to the myocardial dysfunction observed after CPB. (medscape.com)
Ischemic3
- D. odorifera may be a potential candidate drug for treating myocardial ischemic injury. (wjtcm.net)
- Background We previously demonstrated that retinal ischemic perivascular lesions (RIPLs), which are indicative of ischemia in the middle retina, may be a biomarker of ischemic cardiovascular disease. (bvsalud.org)
- The re-establishing of blood flow to an ischemic zone is called reperfusion [ 1 ]. (biomedcentral.com)
Inhibition5
- 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)
- Sirt1 mediates light-induced damage mitigation by HRS through inhibition of apoptosis and oxidant-stress. (arvojournals.org)
- Cardiac I/R induced a marked inhibition of cardiac function and myocardial injury. (phoenixpeptide.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)
Acute4
- Before ischemia, acute troglitazone treatment had no effect on LV function, electrocardiogram, or substrate utilization. (diabetesjournals.org)
- Acute treatment with troglitazone increases susceptibility to ventricular fibrillation during myocardial ischemia and reperfusion. (diabetesjournals.org)
- Therefore, the aim of this study was to investigate apoptosis in various cardiac diseases: in hyperlipidemia induced atherosclerosis, in acute rejected heart transplants, in ischemia and reperfusion as well as in chronic hypoxia. (uni-frankfurt.de)
- [ 6 ] These include multivessel coronary artery spasm, impaired cardiac microvascular function, impaired myocardial fatty acid metabolism, acute coronary syndrome with reperfusion injury, and endogenous catecholamine-induced myocardial stunning and microinfarction. (medscape.com)
Coronary artery1
- DCM is a cardiac pathological condition in patients with DM characterized by the appearance of aberrant myocardial morphology and cardiac functions in the truancy of other factors, such as coronary artery disease, hypertension, and prominent valvular disease [ 3 ] . (encyclopedia.pub)
Left ventricular2
- We previously demonstrated that chronic pretreatment with a thiazolidinedione peroxisome proliferator-activated receptor (PPAR)-γ activator, troglitazone, improves recovery of left ventricular (LV) function and substrate metabolism after ischemia and reperfusion, without causing arrhythmias. (diabetesjournals.org)
- Patients with TCM are found to shift toward the glucose pathway despite relatively normal myocardial perfusion and lack of ischemia in left ventricular segments. (medscape.com)
Ventricular2
- 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)
- 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)
Infarct size7
- The 1- and 2-AR blockers CGP-20712A and ICI-118551 completely abolished the isoproterenol-induced reduction in infarct size and improvement in mechanical recovery, while the 3-AR blocker was without effect. (sun.ac.za)
- Both Rp-8-CPT-cAMPs and wortmannin significantly increased infarct size when administered before 1/ 2-AR preconditioning or at the onset of reperfusion while it reduced mechanical recovery during reperfusion. (sun.ac.za)
- PTX pretreatment had no significant effect on the reduction in infarct size induced by 1/ 2-AR or 2-AR preconditioning, however it reduced mechanical recovery in the latter. (sun.ac.za)
- The NOS inhibitors had no effect on the reduction in infarct size induced by 1/ 2-AR preconditioning, but depressed mechanical function during reperfusion. (sun.ac.za)
- The significant reduction in infarct size by 1/ 2-PC, was associated with activation of ERKp44/p42 and PKB/Akt during the triggering phase, as well as during reperfusion. (sun.ac.za)
- 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)
- 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)
Myocardium2
- The most commonly discussed possible mechanism for TCM is stress-induced catecholamine release, with toxicity to and subsequent stunning of the myocardium. (medscape.com)
- Immature calcium handling in immature myocardium raises intracellular calcium concentrations after ischemia and reperfusion. (medscape.com)
Oxidative7
- 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)
- 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)
- HiChol rat cardiac myocytes showed reduction of cell viability and increased oxidative stress, which were further aggravated by SI/R and with additional hyperglycemia. (nih.gov)
- 1 Although the pathogenesis of light-induced retinal damage remains unclear, oxidative stress is likely involved. (arvojournals.org)
- Thus, treatment targeting mitochondrial-induced oxidative stress is very crucial in suppressing DCM. (encyclopedia.pub)
- In addition, cardiac markers of aging-induced damage, including radical oxidative species levels, mitochondrial metabolic activity, mitochondrial calcium buffer capacity, and estrogenic signaling functions, were also modulated by the compound. (hindawi.com)
- In addition, some pathways that are typically altered during cardiac aging-induced damage, including the generation of radical oxidative species, the mitochondrial metabolic activity, the modulation of the mitochondrial calcium buffering capacity, and the regulation of estradiol and estrogen-regulated gene expression, were investigated [ 20 - 22 ]. (hindawi.com)
Apoptosis in rats1
- Wogonin could suppress apoptosis in rats experienced myocardial I/R [ 25 ]. (hindawi.com)
Endogenous1
- ENGLISH ABSTRACT: The Mechanism of -adrenergic preconditioning ( -PC) Ischaemic preconditioning (IPC), a potent endogenous protective intervention against myocardial ischaemia, is induced by exposure of the heart to repetitive short episodes of ischaemia and reperfusion. (sun.ac.za)
Vitro4
- These results showed that DOEO had significant myocardial cell protection, with IC 50 values ranging from 17.64 to 24.78 μg/mL in vitro . (wjtcm.net)
- This ELISA kit applies to the in vitro quantitative determination of Rat BMG/β2-MG concentrations in serum, plasma and other biological fluids. (elabscience.com)
- Nucleic acid-blocking morpholinos, designed to selectively induce Ceacam1-S, protected hepatocyte cultures against temperature-induced stress in vitro. (bvsalud.org)
- An in vitro model of premature myocardial senescence was established as previously reported [ 19 ]. (hindawi.com)
Damage in rats1
- Renal damage in rats induced by myocardi. (sdu.edu.tr)
Pretreatment5
- Compared to the myocardial ischemia group, the DOEO pretreatment groups had lower levels of myocardial injury, creatinine kinase, lactate dehydrogenase, alanine transaminase, aspartate transaminase, hydrogen peroxide, and nitric oxide, and higher levels of glutathione and superoxide dismutase. (wjtcm.net)
- The results demonstrated that Vitexin pretreatment significantly reduced neuronal apoptosis, and inhibited caspase‑3 activity, apoptosis regulator BAX protein expression and malondialdehyde levels in sevoflurane‑induced newborn rats. (spandidos-publications.com)
- 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)
- Moreover, pretreatment of cardiomyocytes with SAHA resulted in a 4-fold decrease in I/R-induced loss of mitochondrial membrane potential and a 25%-40% reduction in cytosolic ROS levels. (wustl.edu)
- The sympathetic/catecholamine theory is gaining momentum, because TCM was induced in rats exposed to physical stress and, in some instances, was prevented by pretreatment with an alpha blocker or beta blocker. (medscape.com)
Cerebral ischemia1
- Upregulation of HIF-1 expression may play a neuroprotective role in animal models of focal cerebral ischemia ( 6 ). (spandidos-publications.com)
Hypertrophy4
- 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)
- 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)
- 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)
Pathways3
- Overall, the study showed that DOEO displayed myocardial protection by upregulating the NF-E2-related nuclear factor- antioxidant response element (Nrf2-ARE) and caspase pathways. (wjtcm.net)
- the respective roles of the A1-, A2-, A3-adenosine receptors as well as the involvement of the PI3-K/PKB/Akt and ERKp44/p42 signal transduction pathways, in the cardioprotective phenomemon of -adrenergic preconditioning and (iv) the contribution of the mitochondrial KATP channels (mKATP), reactive oxygen species and NO to the mechanism of -AR-induced cardioprotection. (sun.ac.za)
- 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)
Mitochondrial biogenesis1
- Epicatechin induces mitochondrial biogenesis and markers of muscle regeneration in adults with Becker muscular dystrophy. (ucsd.edu)
Sprague-Dawley2
- Thirty male Sprague-Dawley rats were randomly assigned to three groups (10 rats per group): control group, LPS group and LPS + extract group. (biomedcentral.com)
- Anterior MI was induced in Sprague-Dawley rats ( n = 8) and allowed to heal over 2 months. (frontiersin.org)
Hypoxia4
- In murine cardiomyocytes miR-21 was found to protect from hypoxia/reoxygenation (H/R)-induced cell apoptosis via regulation of its target gene PDCD4 [ 13 ]. (hindawi.com)
- Transfection of Ceacam1-deficient mouse hepatocytes with adenoviral Ceacam1-S mitigated hypoxia-induced loss of cellular adhesion by repressing the Ask1/p-p38 cell death pathway. (bvsalud.org)
- Furthermore, it was revealed that treatment with vitexin induced hypoxia inducible factor 1α subunit (HIF‑1α) and vascular endothelial growth factor (VEGF) protein expression, and suppressed phosphorylated‑p38 MAP kinase (p38) protein expression in sevoflurane‑induced newborn rat. (spandidos-publications.com)
- Cardiomyocytes were isolated and subjected to 6 h hypoxia followed by 18 h reperfusion. (biomedcentral.com)
Protects2
- 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)
- In a study published in 2006 in the journal Cell, researchers in France found that resveratrol protects mice against diet-induced insulin resistance and obesity. (lifeextension.com)
Experimental2
- Mehta's thesis topic was "studies on experimental myocardial reperfusion" which he completed under the direction of Prof. Tom Saldeen. (wikipedia.org)
- Accordingly, in our study, we investigated the neuroprotective potential of LIG following experimental SAH in rats. (alexbotsaris.com.br)
Injury induced1
- The comparison showed that the anti-H9c2 cell injury effect of PLR was superior to that of PTR, and the effect of IAF on each pharmacodynamic index was better than that of MS. CONCLUSION PLR and PTR can protect H9c2 cells against injury induced by OGD/R in different degrees, while PLR playing a stronger role, which might be through the regulation of MAPKp38 and NFκBp65 protein expressions. (magtechjournal.com)
Pathway2
- Effect of Gualou Xiebai Decoction on pulmonary fibrosis in rats based on pyroptosis pathway]. (brain-knowledge-engine.org)
- During ischemia, this pathway is suppressed and instead glucose is largely utilized, resulting in impaired cardiac function. (medscape.com)
Cell apoptosis1
- 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)
Mice5
- The myocardial I/R model was established using C57BL/J6 mice. (spandidos-publications.com)
- CNS and behavioral activity of rutin were on hole board, thiopental-induced sleeping time and locomotor activity tests in mice. (fuqna.com)
- Recent studies have shown that the exposure to clinically relevant doses of narcotic drugs, such as isoflurane and sevoflurane, leads to neurological disorders in rats and mice ( 3 , 4 ). (spandidos-publications.com)
- Today, resveratrol is attracting attention for its unique ability to mimic the gene expression effects of caloric restriction, the only intervention that has been shown in peer-reviewed studies to prolong maximum life span and/or produce anti-aging effects in a variety of organisms, including mice, rats, dogs, and monkeys. (lifeextension.com)
- TREM2 Deficiency Aggravates NLRP3 Inflammasome Activation and Pyroptosis in MPTP-Induced Parkinson's Disease Mice and LPS-Induced BV2 Cells. (brain-knowledge-engine.org)
Arrhythmias1
- Reperfusion-induced Arrhythmias and Oxygen-Derived Free Radicals. (aiwo.com)
Methods3
- Methods: Isolated perfused rat hearts were subjected to 35 min regional ischaemia (RI) and reperfusion. (sun.ac.za)
- MATERIALS AND METHODS: ASP (1g/kg) or vehicle (normal saline) was intragastrically administrated to rats everyday for 14d. (alexbotsaris.com.br)
- [ 3 , 4 ] Further refinements in CPB hardware and techniques, perfusion methods, myocardial and brain protection over the past seven decades contributed to improved outcomes of surgical treatment of CHD. (medscape.com)
Isolated rat hearts4
- Effects of intermedin(1-53) on cardiac function and ischemia/reperfusion injury in isolated rat hearts. (phoenixpeptide.com)
- The present study was designed to observe the effects of IMD(1-53) on cardiac function in ischemia/reperfusion (I/R) injury in isolated rat hearts. (phoenixpeptide.com)
- Protective effects of intermedin/adrenomedullin2 on ischemia/reperfusion injury in isolated rat hearts. (phoenixpeptide.com)
- Isolated rat hearts were perfused on a Langendorff apparatus and subjected to 45-min global ischemia and 30-min reperfusion. (phoenixpeptide.com)
Lipopolysaccharide2
- The aim of this work was to investigate the effect of the extract from Agkistrodon halys venom on lipopolysaccharide (LPS)-induced myocardial injury. (biomedcentral.com)
- Lipopolysaccharide (LPS), a bacterial endotoxin located in the outer membrane of the cell wall of the Gram-negative bacteria, is considered as the principal factor responsible for multiple organs damage including myocardial injury in patients with sepsis [ 2 , 3 ]. (biomedcentral.com)
Lactate3
- In addition, reperfusion with IMD(1-53)markedly attenuated the leakage of lactate dehydrogenase and malondialdehyde content in myocardia compared with I/R alone. (phoenixpeptide.com)
- The release of myocardial protein and lactate dehydrogenase (LDH) and the formation of malondialdehyde (MDA) were assayed. (phoenixpeptide.com)
- The uncoupling of glycolysis and glucose oxidation induces lactate accumulation during myocardial ischemia/reperfusion (I/R) injury. (biomedcentral.com)
SIRT13
- miR‑132 was significantly upregulated and SIRT1 was markedly downregulated in I/R myocardial tissues. (spandidos-publications.com)
- In the present study, we investigated whether Sirtuin Type 1 (Sirt1), a class III histone deacetylase, mediates the retinal protective effect of HRS in rats with light-induced retinal damage. (arvojournals.org)
- Rats were treated with HRS for 5 days after intense light exposure, and then ERGs were performed and retinas were collected to evaluate the effect of HRS on Sirt1 expression. (arvojournals.org)
Cardioprotective effects2
- The cardioprotective effects of DOEO were examined by histopathological observation, myocardial enzyme detection, peroxidation, anti-oxidant level detection, and related protein expression. (wjtcm.net)
- These results suggest that IMD(1-53), like adrenomedullin, has cardioprotective effects against myocardial I/R injury. (phoenixpeptide.com)
Mechanisms3
- 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)
Inhibits1
- IFN-gamma activates macrophages, enhances NK activity and B cell maturation, proliferation and Ig secretion, induces MHC class I and II antigens, and inhibits osteoclast activation. (rndsystems.com)
Myocytes2
- Cardiac myocytes isolated from neonatal or adult rat hearts were cultured in control or in three different hypercholesterolemic media with increasing cholesterol content (hiChol) or hiChol + hyperglycemic medium, respectively. (nih.gov)
- Transmission electron microscopy demonstrated more severely damaged mitochondria and ultrastructural damage to myocytes in Ovx rat hearts. (illinois.edu)
Inflammation2
- The myocardial apoptosis and inflammation have been recognized as features of I/R injury. (hindawi.com)
- Rutin caused attenuation of streptozotocin-induced inflammation by decreasing the activity of the glial fibrillary acidic protein, interleukin-8, cyclooxygenase-2, inducible nitric oxide synthase and nuclear factor-kB and thereby prevented gross anatomical changes in rat hippocampus. (fuqna.com)
Autophagy2
- Donepezil attenuated cardiac ischemia/reperfusion injury through balancing mitochondrial dynamics, mitophagy, and autophagy[J]. Transl Res, 2021,230:82-97. (magtechjournal.com)
- 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)
Cardiac function2
- Reperfusion treatment has a potential risk of worsening tissue damage after ischemia, which can accelerate the deterioration of cardiac function [ 2 ]. (hindawi.com)
- Reperfusion with IMD(1-53) significantly ameliorated the inhibited cardiac function and bradycardia induced by I/R. Compared with the I/R-treatment alone, IMD(1-53) reperfusion augmented CPF, LVSP, and maximal rate of increase and decrease of left ventricle pressure (+/-LVdP/dt(max)) and decreased LVDP. (phoenixpeptide.com)
Serum4
- 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)
- This Rat cTn-I ELISA Kit was designed for the quantitative measurement of Rat cTn-I protein in serum, plasma, tissue homogenates. (cusabio.com)
- Cholesterol diet did not induce morphological changes of the aortas in spite of elevated serum cholesterol. (uni-frankfurt.de)
Suppress1
- CONCLUSIONS: ASP can suppress the expression of hepcidin in normal rats, and may be used in the treatments of hepcidin-induced diseases. (alexbotsaris.com.br)
Diabetic1
Neuroprotective1
- Rutin has demonstrated the neuroprotective effect on brain ischemia. (fuqna.com)
Significantly1
- Reperfusion with IMD significantly attenuated the I/R injury. (phoenixpeptide.com)
Heart5
- 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)
- Later, he went on to show that platelets also have a protective effect on the heart during ischemia mediated through release of transforming growth factor ß1. (wikipedia.org)
- Epicatechin Ameliorates Cardiac Fibrosis in a Female Rat Model of Pre-Heart Failure with Preserved Ejection Fraction. (ucsd.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)
- With ischemia in coronary heart disease, impairment of the oxygen supply and metabolic disorder both occur [ 2 ]. (biomedcentral.com)
Concentrations1
- To assess the linearity of the assay, samples were spiked with high concentrations of rat cTn-Ⅰ in various matrices and diluted with the Sample Diluent to produce samples with values within the dynamic range of the assay. (cusabio.com)
Protective effects3
- 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)
- Conversely, blocking miR-21 expression with miR-21 inhibitor effectively suppressed the protective effects of TFs against H/R-induced injury. (hindawi.com)
- Interestingly, the above IMD effects were similar to those of adrenomedullin (10(-8)mol/L). These results suggest that IMD, like adrenomedullin, exerts cardio-protective effects against myocardial I/R injury. (phoenixpeptide.com)
Treatment4
- 3 - 5 Therefore, antioxidants capable of easily passing the blood-retinal barrier could be a promising treatment for light-induced damage. (arvojournals.org)
- In a study, in haloperidol-induced orofacial dyskinesia, rutin treatment reversed behavioral changes such as orofacial dyskinetic movements, stereotypic rearing, locomotor activity, and percent retention along with restoration of biochemical and neurochemical parameters. (fuqna.com)
- Rats with SAH induced using the established double hemorrhage model were administered with or without LIG treatment. (alexbotsaris.com.br)
- We provide a new insight into this potential drug for the treatment of myocardial I/R injury. (biomedcentral.com)
Senescence1
- through bioinformatics, we found that nlrp3 , gsdmd , il-1\xce\xb2and other hub proteins of pyroptosis were highly expressed in ivdd sd rats, and network pharmacology discovered that dhjsd may control cellular senescence, apoptosis, and pyroptosis in order to treat ivdd. (brain-knowledge-engine.org)
Spinal1
- 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)
Reduction1
- 0.05) dilation of the left ventricle, and reduction in ejection fraction compared to sham operated rats ( n = 4) on 7 T cardiac magnetic resonance imaging. (frontiersin.org)
Tissues2
- Haematoxylin and eosin staining was performed to observe the injury of myocardial tissues. (spandidos-publications.com)
- Can ferroptosis be specifically induced in tumors but not in normal tissues? (nature.com)
Therapeutic2
- His work on LOX-1 receptors, its polymorphic variants and its role in atherogenesis and myocardial ischemia has led to new therapeutic targets now being pursued by several biotech companies, such as MedImmune. (wikipedia.org)
- A therapeutic drug that targets ischemia reperfusion (I/R) injury is needed and has yet to be developed. (biomedcentral.com)
19931
- 1993. Methylene chloride-induced turmorigenesis. (cdc.gov)
Effect3
- This study aimed to determine the potential myocardial protective effect and possible mechanism of action of D. odorifera essential oil (DOEO). (wjtcm.net)
- Abstract : OBJECTIVE To explore the similarities and differences of material basis, action, and mechanism of Puerariae Lobatae Radix(PLR) and Puerariae Thomsonii Radix(PTR) against myocardial cell injury, and compare the differences of relative amount of active ingredients and the effect against H9c2 cells OGD/R injury in different medicated systems. (magtechjournal.com)
- The present study was designed to determine the protective effect of IMD on cardiac ischemia/reperfusion (I/R) injury and its possible mechanism. (phoenixpeptide.com)