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epicatechin/accident vasculaire cérébral
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The flavanol (-)-epicatechin prevents stroke damage through the Nrf2/HO1 pathway.
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Epidemiologic studies have shown that foods rich in polyphenols, such as flavanols, can lower the risk of ischemic heart disease; however, the mechanism of protection has not been clearly established. In this study, we investigated whether epicatechin (EC), a flavanol in cocoa and tea, is protective
Metformin treatment in the period after stroke prevents nitrative stress and restores angiogenic signaling in the brain in diabetes.
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Diabetes impedes vascular repair and causes vasoregression in the brain after stroke, but mechanisms underlying this response are still unclear. We hypothesized that excess peroxynitrite formation in diabetic ischemia/reperfusion (I/R) injury inactivates the p85 subunit of phosphoinositide 3-kinase
Dietary epicatechin intake and 25-y risk of cardiovascular mortality: the Zutphen Elderly Study.
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Prospective cohort studies have shown that the consumption of cocoa and tea is associated with lower risk of cardiovascular diseases (CVDs), and cocoa and tea have been shown to improve CVD risk factors in randomized controlled trials. Cocoa and tea are major dietary sources of the flavan-3-ol
Protein nitration impairs the myogenic tone of rat middle cerebral arteries in both ischemic and nonischemic hemispheres after ischemic stroke.
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The myogenic response is crucial for maintaining vascular resistance to achieve constant perfusion during pressure fluctuations. Reduced cerebral blood flow has been reported in ischemic and nonischemic hemispheres after stroke. Ischemia-reperfusion injury and the resulting oxidative stress impair
Epicatechin gallate increases glutamate uptake and S100B secretion in C6 cell lineage.
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There is a current interest in dietary compounds, such as green tea polyphenols, that can favor protection against a variety of brain disorders, including Alzheimer's disease, ischemia, and stroke. The objective of the present study was to investigate the effects of (-)-epicatechin-3-gallate (ECG),
Therapeutic Targets of Oxidative/Nitrosative Stress and Neuroinflammation in Ischemic Stroke: Applications for Natural Product Efficacy with Omics and Systemic Biology.
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Oxidative/nitrosative stress and neuroinflammation are critical pathological processes in cerebral ischemia-reperfusion injury, and their intimate interactions mediate neuronal damage, blood-brain barrier (BBB) damage and hemorrhagic transformation (HT) during ischemic stroke. We review current
Synergistic neuroprotection by epicatechin and quercetin: Activation of convergent mitochondrial signaling pathways.
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In view of evidence that increased consumption of epicatechin (E) and quercetin (Q) may reduce the risk of stroke, we have measured the effects of combining E and Q on mitochondrial function and neuronal survival following oxygen-glucose deprivation (OGD). Relative to mouse cortical neuron cultures
Molecular Mechanisms and Therapeutic Effects of (-)-Epicatechin and Other Polyphenols in Cancer, Inflammation, Diabetes, and Neurodegeneration.
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With recent insight into the mechanisms involved in diseases, such as cardiovascular disease, cancer, stroke, neurodegenerative diseases, and diabetes, more efficient modes of treatment are now being assessed. Traditional medicine including the use of natural products is widely practiced around the
Oral administration of the flavanol (-)-epicatechin bolsters endogenous protection against focal ischemia through the Nrf2 cytoprotective pathway.
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Consumption of flavan-3-ols, notably (-)-epicatechin (EC), has been highly recommended in complementary and alternative medicine (CAM) due to reports that flavan-3-ols boost antioxidant activity, support vascular function, and prevent cardiovascular disease. To date, in vivo efficacy and mechanisms
(-)-Epicatechin protects hemorrhagic brain via synergistic Nrf2 pathways.
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OBJECTIVE
In the wake of intracerebral hemorrhage (ICH), a devastating stroke with no effective treatment, hemoglobin/iron-induced oxidative injury leads to neuronal loss and poor neurologic outcomes. (-)-Epicatechin (EC), a brain-permeable flavanol that modulates redox/oxidative stress via the
(-)-Epicatechin, a Natural Flavonoid Compound, Protects Astrocytes Against Hemoglobin Toxicity via Nrf2 and AP-1 Signaling Pathways.
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(-)-Epicatechin is a brain-permeable, natural product found at high concentrations in green tea and cocoa. Our previous research has shown that (-)-epicatechin treatment reduces hemorrhagic stroke injury via nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway in vivo. However, the
Cerebroprotection of flavanol (-)-epicatechin after traumatic brain injury via Nrf2-dependent and -independent pathways.
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Traumatic brain injury (TBI), which leads to disability, dysfunction, and even death, is a prominent health problem worldwide with no effective treatment. A brain-permeable flavonoid named (-)-epicatechin (EC) modulates redox/oxidative stress and has been shown to be beneficial for vascular and
An in vitro hyperbaric oxygen system for evaluation of free radical damage and protection by catechins on hemorheological parameters.
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Free radicals play a critical role in causing hemorheologic abnormality which is highly correlated with cardiovascular disease and stroke. In this study, we established an in vitro model to evaluate the influence of free radical attacks on hemorheological parameters. A well-sealed chamber with
Assessment of the polyphenolic composition of the organic extracts of Mauritian black teas: a potential contributor to their antioxidant functions.
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There is increasing interest in the emerging view that tea improves the antioxidant status in vivo and thereby helps to lower risk of certain types of cancer, coronary heart disease and stroke and its component biofactors could provide prophylactic potential for these diseases. The polyphenolic
Efficacy of prophylactic flavan-3-ol in permanent focal ischemia in 12-mo-old mice.
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The consumption of flavan-3-ol-containing foods, including (-)-epicatechin (EC), has been linked to lower incidence of cardiovascular disease and stroke. We previously demonstrated nuclear transcription factor erythroid 2p45-related factor-2 (Nrf2) -dependent EC efficacy in reducing stroke-induced
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