epicatechin/necroză

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(-)-Epicatechin in the prevention of tumor necrosis alpha-induced loss of Caco-2 cell barrier integrity.

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An increased permeability of the intestinal barrier is proposed as a major event in the pathophysiology of inflammatory bowel diseases (IBD). Tumor necrosis alpha (TNFα) plays a central role in IBD pathogenesis, in part promoting tight function (TJ) barrier dysfunction. Food extracts enriched in

Flavonoids as inhibitors or enhancers of the cytotoxicity of tumor necrosis factor-alpha in L-929 tumor cells.

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The effects of some selected flavonoids on tumor necrosis factor-alpha (TNF)-induced cytotoxicity in murine fibroblast L-929 cells were studied. All of the flavanones tested as well as a flavan, epicatechin, protected L-929 cells from TNF-induced cell death of the flavanones tested, hesperetin,

Epicatechin administration leads to necrotic cell death of rat leukaemia promyelocytes in vivo.

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BACKGROUND (-)-Epicatechin (EC) induces oxidative DNA damage in HL-60 cells. The association between genotoxic and apoptotic/necrotic effects of EC was studied in rats with acute myeloid leukaemia. METHODS Healthy and leukaemic rats were given EC by oral gavage at a dose of 40 mg/kg body weight for

Evaluation of the Anti-apoptotic and Anti-cytotoxic Effect of Epicatechin Gallate and Edaravone on SH-SY5Y Neuroblastoma Cells

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Introduction: Parkinson disease (PD) is the second most common neurodegenerative disease affecting older individuals with signs of motor disability and cognitive impairment. Epicatechin (EC) and edaravone have neuroprotective effects most probably due to their

Sex- and strain-dependent effects of epigallocatechin gallate (EGCG) and epicatechin gallate (ECG) in the mouse.

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We have previously demonstrated that 50mg/kg of epigallocatechin gallate (EGCG) is hepatotoxic to female Swiss Webster mice, while lower doses of EGCG and epicatechin gallate (ECG) modulate various cytochrome P450 (CYP) isoforms. Therefore, this study was designed to further investigate the role of

A pilot study on clinical pharmacokinetics and preclinical pharmacodynamics of (+)-epicatechin on cardiometabolic endpoints.

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We reported that (-)-epicatechin can stimulate mitochondria biogenesis and improve metabolism. However, preliminary studies indicate that the (+) stereoisomer form may be more potent. We evaluated in a preliminary manner, the pharmacokinetics (PK) and initial safety analysis of (+)-epicatechin

Immunomodulatory effects of epicatechin-(2β→O→7, 4β→8)-ent-epicatechin isolated from Rhododendron spiciferum in vitro.

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BACKGROUND Many traditional Chinese medicines (TCMs) can act as either immunosuppresants or immunostimulants, properties that have lead to their increasing use as immunomodulators in the treatment of disease. Recently, our lab successfully identified a dimer epicatechin-(2β→O → 7,

(-)-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

Dietary flavonoids attenuate tumor necrosis factor alpha-induced adhesion molecule expression in human aortic endothelial cells. Structure-function relationships and activity after first pass metabolism.

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Flavonoids have been suggested to exert human health benefits by anti-oxidant and anti-inflammatory mechanisms. In this study, we investigated whether and by what mechanisms dietary flavonoids inhibit expression of cellular adhesion molecules, which is relevant to inflammation and atherosclerosis.

Tea polyphenols inhibit IL-6 production in tumor necrosis factor superfamily 14-stimulated human gingival fibroblasts.

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IL-6 is well recognized to be a potent bone resorptive agent and thus in the development of periodontal disease. Epigallocatechin gallate (EGCG) and epicatechin gallate (ECG), the major catechins in green tea, and theaflavin-3,3'-digallate (TFDG), polyphenol in black tea, have multiple beneficial

(-)-Epicatechin Reduces Blood Pressure and Improves Left Ventricular Function and Compliance in Deoxycorticosterone Acetate-Salt Hypertensive Rats.

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(−)-Epicatechin (E) is a flavanol found in green tea and cocoa and has been shown to attenuate tumour necrosis factor alpha (TNF-α)-mediated inflammation, improve nitric oxide levels, promote endothelial nitric oxide synthase (eNOS) activation and inhibit NADPH oxidase. This study

Anti-arthritic and anti-inflammatory effects of (-)-Epicatechin-3-O-β-d-allopyranoside, a constituent of Davallia formosana.

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(-)-Epicatechin-3-O-β-d-allopyranoside (ECAP) is isolated from the popular Chinese herbal medicine Davallia formosana, which has been used to treat bone diseases including bone fracture, arthritis, and osteoporosis.To investigate the antiarthritic and the

(-)-Epicatechin protects thoracic aortic perivascular adipose tissue from whitening in high-fat fed mice

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High adipose tissue (AT) accumulation in the body increases the risk for many metabolic and chronic diseases. This work investigated the capacity of the flavonoid (-)-epicatechin to prevent undesirable modifications of AT in mice fed a high-fat diet. Studies were focused on thoracic aorta

(-)-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.

(-)-Epicatechin protects the intestinal barrier from high fat diet-induced permeabilization: Implications for steatosis and insulin resistance.

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Increased permeability of the intestinal barrier is proposed as an underlying factor for obesity-associated pathologies. Consumption of high fat diets (HFD) is associated with increased intestinal permeabilization and increased paracellular transport of endotoxins which can promote steatosis and

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