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epicatechin/tulehdus
Linkki tallennetaan leikepöydälle
Sivu 1 alkaen 338 tuloksia
LPS-induced renal inflammation is prevented by (-)-epicatechin in rats.
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This work investigated the capacity of (-)-epicatechin to prevent the renal damage induced by LPS administration in rats. Male Sprague Dawley rats were fed for 4 days a diet without or with supplementation with (-)-epicatechin (80mg/kg BW/d), and subsequently i.p. injected with lipopolysaccharide
Protective effect of Epicatechin on APAP-induced acute liver injury of mice through anti-inflammation and apoptosis inhibition.
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Epicatechin (EC) is the most effective compound in Euonymus alatus (Thunb.)Sieb, and possesses a series of benefits, including anti-inflammatory, antioxidant, antiobesity and anticancer effects. In this study, we investigated the protective effects of EC in Acetaminophen(N-acetyl-p-aminophenol,
Antinociceptive effect of (-)-epicatechin in inflammatory and neuropathic pain in rats.
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The aim of this study was to investigate the antinociceptive potential of (-)-epicatechin and the possible mechanisms of action involved in its antinociceptive effect. The carrageenan and formalin tests were used as inflammatory pain models. A plethysmometer was used to measure inflammation and
Epicatechin and scopoletin rich Morinda citrifolia (Noni) leaf extract supplementation, mitigated Osteoarthritis via anti-inflammatory, anti-oxidative, and anti-protease pathways.
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The scopoletin (coumarin) and epicatechin (flavonoid) rich Morinda citrifolia L. (MC) Noni leaves are non-toxic (unlike the fruits) and consumed as vegetables. The anti-osteoarthritis effects of the MC leaf extract against joint cartilage degradation and inflammation were investigated through
Epicatechin and scopoletin-rich Morinda citrifolia leaf ameliorated leukemia via anti-inflammatory, anti-angiogenesis, and apoptosis pathways in vitro and in vivo.
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The anti-leukemia mechanisms of Morinda citrifolia L. leaf extract were investigated on human Jurkat leukemia cells and in leukemia-induced BALB/c mice. The leukemia-induced mice were fed daily with the extract (100 or 200 mg/kg BW) and compared to ATRA (All-trans-retinoic-acid; 5 mg/kg BW). After 4
(-)-Epicatechin and the colonic metabolite 2,3-dihydroxybenzoic acid protect against high glucose and lipopolysaccharide-induced inflammation in renal proximal tubular cells through NOX-4/p38 signalling
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Chronic hyperglycaemia and inflammation are present in diabetes and both processes have been related to the pathogenesis of diabetic kidney disease. Epicatechin (EC) and main colonic phenolic acids derived from flavonoid intake, such as 2,3-dihydroxybenzoic acid (DHBA), 3,4-dihydroxyphenylacetic
Synthesis of (-)-epicatechin 3-(3-O-methylgallate) and (+)-catechin 3-(3-O-methylgallate), and their anti-inflammatory activity.
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A concise synthesis of (-)-epicatechin 3-(3-O-methylgallate) (1; ECG3''Me), which is a minor constituent of tea, and (+)-catechin 3-(3-O-methylgallate) (2; CG3''Me) via condensation of equimolar amount of catechin and gallate derivatives has been achieved. The anti-inflammatory effect of the
Anti-arthritic and anti-inflammatory effects of (-)-Epicatechin-3-O-β-d-allopyranoside, a constituent of Davallia formosana.
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(-)-Epicatechins promote vascular health through epigenetic reprogramming of endothelial-immune cell signaling and reversing systemic low-grade inflammation.
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Ingestion of (-)-epicatechin flavanols reverses endothelial dysfunction by increasing flow mediated dilation and by reducing vascular inflammation and oxidative stress, monocyte-endothelial cell adhesion and transendothelial monocyte migration in vitro and in vivo. This involves multiple changes in
Analgesic and anti-inflammatory activities of epicatechin gallate from Bauhinia hookeri.
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Hit, Lead & Candidate Discovery The acetic acid-induced writhing and hot plate models in mice were utilized to determine the analgesic effect of epicatechin gallate (ECG) isolated from Bauhinia hookeri. The anti-inflammatory activity of ECG was determined using carrageenan-induced paw edema model.
Epicatechin used in the treatment of intestinal inflammatory disease: an analysis by experimental models.
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Background. This study was pathway of (-)-epicatechin (EC) in the prevention and treatment of intestine inflammation in acute and chronic rat models. Methods. Intestine inflammation was induced in rats using TNBS. The morphological, inflammatory, immunohistochemical, and immunoblotting
(-)-Epicatechin prevents TNFα-induced activation of signaling cascades involved in inflammation and insulin sensitivity in 3T3-L1 adipocytes.
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Obesity is major public health concern worldwide and obese individuals exhibit a higher risk of chronic diseases such as type 2 diabetes. Inflammation plays a significant role in metabolic regulation and mounting evidence highlight the contribution of adipose tissue to systemic inflammatory state.
Dietary (-)-epicatechin mitigates oxidative stress, NO metabolism alterations, and inflammation in renal cortex from fructose-fed rats.
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High fructose consumption has been associated to deleterious metabolic conditions. In the kidney, high fructose causes renal alterations that contribute to the development of chronic kidney disease. Evidence suggests that dietary flavonoids have the ability to prevent/attenuate risk factors of
Directly interact with Keap1 and LPS is involved in the anti-inflammatory mechanisms of (-)-epicatechin-3-gallate in LPS-induced macrophages and endotoxemia.
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Disruption of the Kelch-like ECH-associated protein 1 (Keap1)-Nuclear factor erythroid-derived factor 2-related factor 2 (Nrf2) interaction has emerged as a promising strategy to reduce oxidative stress-induced inflammation. However, its roles in regulating downstream events, including the cross
(-)-Epicatechin attenuates hepatic sinusoidal obstruction syndrome by inhibiting liver oxidative and inflammatory injury.
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Hepatic sinusoidal obstruction syndrome (HSOS) is a rare liver disease with considerable morbidity and mortality. (-)-Epicatechin (EPI) is a natural flavonol. This study aims to investigate the protection of EPI against monocrotaline (MCT)-induced HSOS and its engaged mechanism. Results of serum
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