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ellagic acid/infarkti
Linkki tallennetaan leikepöydälle
Sivu 1 alkaen 17 tuloksia
Ellagic acid inhibits cardiac arrhythmias, hypertrophy and hyperlipidaemia during myocardial infarction in rats.
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OBJECTIVE
The objective was to evaluate the protective effect of ellagic acid against experimentally induced cardiac arrhythmias, hypertrophy and its association with altered lipid metabolism during myocardial infarction in rats.
METHODS
Rats were treated with ellagic acid (7.5 and 15 mg/kg) orally
Ellagic acid promotes ventricular remodeling after acute myocardial infarction by up-regulating miR-140-3p.
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In the paper, we observed the effect of ellagic acid (EA) on myocardial morphology and cardiac function and explored the mechanism of miR-140-3p-mediated EA in ventricular remodeling. The experimental animals were divided into 3 groups: control group, AMI group, AMI+EA group. Intragastric
Experimental studies on the production of pulmonary infarction. IV. Effects of UK, heparin, t-AMCHA or ellagic acid.
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Ellagic acid inhibits oxidized low-density lipoprotein (OxLDL)-induced metalloproteinase (MMP) expression by modulating the protein kinase C-α/extracellular signal-regulated kinase/peroxisome proliferator-activated receptor γ/nuclear factor-κB (PKC-α/ERK/PPAR-γ/NF-κB) signaling pathway in endothelial cells.
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Previous studies have shown that vascular endothelium-derived matrix metalloproteinases (MMPs) contribute to the destabilization of atherosclerotic plaques, a key event triggering acute myocardial infarction. In addition, studies have reported that the PKC-MEK-PPARγ signaling pathway is involved in
Preventive effect of argatroban on ellagic acid-induced cerebral thromboembolism in rats.
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The preventive effect of argatroban, a synthetic thrombin inhibitor, on cerebral infarction was evaluated with ellagic acid (EA)-induced cerebral thromboembolism in rats. Platelet-rich thrombi containing fibrin and EA crystal were formed in the microarteries in the affected hemisphere by the
Mechanistic clues in the protective effect of ellagic acid against apoptosis and decreased mitochondrial respiratory enzyme activities in myocardial infarcted rats.
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Our previous study described the cardioprotective effects of ellagic acid in an isoproterenol-induced myocardial infarction model. In this study, we are reporting the mechanism of protective action of ellagic acid with respect to apoptosis and mitochondrial respiratory enzymes. Ellagic acid (7.5 and
Protective efficacy of ellagic acid on glycoproteins, hematological parameters, biochemical changes, and electrolytes in myocardial infarcted rats.
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The cardioprotective property of ellagic acid in rats has been reported previously. The present study reveals the protective role of ellagic acid in biochemical parameters including serum iron, plasma iron binding capacity, uric acid, glycoprotein, and electrolytes along with hematological
Ellagic acid improves endogenous neural stem cells proliferation and neurorestoration through Wnt/β-catenin signaling in vivo and in vitro.
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The aim of this study is to research the effects of the polyphenol ellagic acid (EA) on brain cells and to explore its mechanism of action, and to evaluate whether EA can be safely utilized by humans as a functional food or therapeutic agent.
A photothrombosis-induced model of brain injury in rats
Pharmacodynamics of ellagic acid on cardiac troponin-T, lyosomal enzymes and membrane bound ATPases: mechanistic clues from biochemical, cytokine and in vitro studies.
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The anti lipid peroxidative and antioxidant effects of ellagic acid against isoproterenol-induced myocardial infarcted rats were reported previously. This study was designed to evaluate the protective effects of ellagic acid on the levels of cardiac troponin-T, lysosomal enzymes, and membrane bound
Ellagic acid-induced thrombotic focal cerebral ischemic model in rats.
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BACKGROUND
Ischemic stroke is a common cause of human disability and death. Animal models of focal cerebral ischemia are widely utilized to mimic human ischemic stroke. Although models of focal cerebral ischemia have been well established, very few evidence is based on triggering the intrinsic
Pharmacodynamic Effect of Ellagic Acid on Ameliorating Cerebral Ischemia/Reperfusion Injury.
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Cerebral ischemia/reperfusion (I/R) injury causes a larger population of disable patients and deaths annually. Three Tibetan prescriptions have been applied in alleviating the I/R injury for a 1,000 years. Interestingly, ellagic acid (EA) is one of the commonly dominated phytochemicals in these 3
Ellagic acid protects against neuron damage in ischemic stroke through regulating the ratio of Bcl-2/Bax expression.
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An oxygen-glucose deprivation and reoxygenation model in primary cultured rat cortical neurons was developed for this study to investigate the effects of ellagic acid (EA), a low-molecular-weight polyphenol, on neuron cells and their function, and to evaluate whether EA can be safely utilized by
Ellagic acid ameliorates isoproterenol induced oxidative stress: Evidence from electrocardiological, biochemical and histological study.
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The present study was designed to evaluate the cardioprotective effects of ellagic acid against isoproterenol induced myocardial infarction in rats by studying electrocardiography, blood pressure, cardiac markers, lipid peroxidation, antioxidant defense system and histological changes. Male Wistar
Ellagic acid inhibits proliferation and migration of cardiac fibroblasts by down-regulating expression of HDAC1.
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Cardiac fibroblasts (CFs) could be activated after myocardial infarction (MI). Thus, it is necessary to explore effective drugs to suppress the activation of CFs following MI. This study was designed to investigate the impacts of ellagic acid on CFs and the underlying mechanisms. The expression of
Urolithin A Prevents Focal Cerebral Ischemic Injury via Attenuating Apoptosis and Neuroinflammation in Mice
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Neuroinflammation contributes to neuronal death in cerebral ischemia. Urolithin A (UA), a gut microbial metabolite of ellagic acid, has emerged as a potential anti-inflammatory agent. However, its roles and precise mechanisms in stroke remain unknown. Here we found that UA treatment ameliorated
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