Tea, flavonoids, and cardiovascular health: endothelial protection

Grassi, Davide; Desideri, Giovambattista; Giosia, Paolo Di; Feo, Martina De; Fellini, Emanuela; Cheli, Paola; Ferri, Livia; Ferri, Claudio

doi:10.3945/ajcn.113.058313

Cited by 89 publications

(66 citation statements)

References 54 publications

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“…Flavonoids have repeatedly been shown to improve cardiovascular diseases including hypertension, ischemic heart disease, and stroke (Hertog et al, 1993;Keli et al, 1996;Perez-Vizcaino et al, 2009). It has been further shown that flavonoids protect and improve endothelial function (Engler et al, 2004;Vita, 2005;Hodgson, 2006;Grassi et al, 2013). This is of considerable importance because endothelial dysfunction is a hallmark of most types of cardiovascular disease, including hypertension, diabetes, atherosclerosis, and ischemic heart disease (Hadi et al, 2005;Vita, 2005;Deanfield et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

Luteolinidin Protects the Postischemic Heart through CD38 Inhibition with Preservation of NAD(P)(H)

Boslett

Hemann

Zhao

et al. 2017

J Pharmacol Exp Ther

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We recently showed that ischemia/reperfusion (I/R) of the heart causes CD38 activation with resultant depletion of the cardiac NADP(H) pool, which is most marked in the endothelium. This NADP(H) depletion was shown to limit the production of nitric oxide by endothelial nitric oxide synthase (eNOS), which requires NADPH for nitric oxide production, resulting in greatly altered endothelial function. Therefore, intervention with CD38 inhibitors could reverse postischemic eNOS-mediated endothelial dysfunction. Here, we evaluated the potency of the CD38 inhibitor luteolinidin, an anthocyanidin, at blocking CD38 activity and preserving endothelial and myocardial function in the postischemic heart. Initially, we characterized luteolinidin as a CD38 inhibitor in vitro to determine its potency and mechanism of inhibition. We then tested luteolinidin in the ex vivo isolated heart model, where we determined luteolinidin uptake with aqueous and liposomal delivery methods. Optimal delivery methods were then further tested to determine the effect of luteolinidin on postischemic NAD(P)(H) and tetrahydrobiopterin levels. Finally, through nitric oxide synthase-dependent coronary flow and left ventricular functional measurements, we evaluated the efficacy of luteolinidin to protect vascular and contractile function, respectively, after I/R. With enhanced postischemic preservation of NADPH and tetrahydrobiopterin, there was a dose-dependent effect of luteolinidin on increasing recovery of endothelium-dependent vasodilatory function, as well as enhancing the recovery of left ventricular contractile function with increased myocardial salvage. Thus, luteolinidin is a potent CD38 inhibitor that protects the heart against I/R injury with preservation of eNOS function and prevention of endothelial dysfunction.

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Section: Discussionmentioning

confidence: 99%

Luteolinidin Protects the Postischemic Heart through CD38 Inhibition with Preservation of NAD(P)(H)

Boslett

Hemann

Zhao

et al. 2017

J Pharmacol Exp Ther

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“…[1][2][3][4] As a result, catechin and EGCG have attracted the interest of researchers and manufacturers, and these natural molecules are considered to be promising drug candidates in the pharmaceutical, cosmetic, and nutritional fields. They have already been used in the food industry as natural additives and have been applied in cosmetic products as antiaging components.…”

Section: Introductionmentioning

confidence: 99%

Enhanced uptake and transport of (+)-catechin and (-)-epigallocatechin gallate in niosomal formulation by human intestinal Caco-2 cells

Song

Zhou

et al. 2014

IJN

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The aim of this study was to evaluate (+)-catechin and (−)-epigallocatechin gallate (EGCG) cellular uptake and transport across human intestinal Caco-2 cell monolayer in both the absence and presence of niosomal carrier in variable conditions. The effect of free drugs and drug-loaded niosomes on the growth of Caco-2 cells was studied. The effects of time, temperature, and concentration on drug cellular uptake in the absence or presence of its niosomal delivery systems were investigated. The intestinal epithelial membrane transport of the drug-loaded niosomes was examined using the monolayer of the human Caco-2 cells. The kinetics of transport, and the effect of temperature, adenosine triphosphate inhibitor, permeability glycoprotein inhibitor, multidrug resistance-associated protein 2 inhibitor, and the absorption enhancer on transport mechanism were investigated. It was found that the uptake of catechin, EGCG, and their niosomes by Caco-2 cells was 1.22±0.16, 0.90±0.14, 3.25±0.37, and 1.92±0.22 μg/mg protein, respectively (n=3). The apparent permeability coefficient values of catechin, EGCG, and their niosomes were 1.68±0.16, 0.88±0.09, 2.39±0.31, and 1.42±0.24 cm/second (n=3) at 37°C, respectively. The transport was temperature- and energy-dependent. The inhibitors of permeability glycoprotein and multidrug resistance-associated protein 2 and the absorption enhancer significantly enhanced the uptake amount. Compared with the free drugs, niosomal formulation significantly enhanced drug absorption. Additionally, drug-loaded niosomes exhibited stronger stability and lower toxicity. These findings showed that the oral absorption of tea flavonoids could be improved by using the novel drug delivery systems.

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“…Therefore, it could help to protect against the development and progression of cardiovascular disease (31). Antioxidant actions would be at the root of its biological activity but other mechanisms could also play an important role (32,33).…”

Section: Discussionmentioning

confidence: 99%

ALPHA ANTIADRENERGIC EFFECT OF Achyrocline bogotensis EXTRACT (“Vira Vira”) IN ISOLATED RAT AORTIC RING

Lara

Rincón

Guerrero

2017

Vitae

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Background: The treatment of symptoms of prostatic hyperplasia is among the traditional uses of Achyrocline bogotensis (Kunth) [N.V. "Vira Vira", Compositae] in Colombia. Pharmacological therapy for this disorder depends mainly on alpha-1 antiadrenergic agents, and the mechanism has not been studied previously using A. bogotensis. Objectives: To assess the alpha-1 antiadrenergic effect of the extract obtained from the aerial parts of A. bogotensis in isolated aortic rings from Wistar rats. Methods: The study compared the effects of the ethanol extract of A. bogotensis, prazosin (reference) and DMSO (control) in rings stimulated with phenylephrine (PE) or KCl. The capacity to reduce the PE pressor effect by the ethanol extract (pD 2 ' value) was determined. To quantify the A. bogotensis relaxant potency, increasing concentrations of the ethanol extract (0.1 µg/mL-0.1 mg/mL), were added cumulatively to isolated aortic rings pre-contracted with PE (0.1 µM) or KCl (80 mM). To explore the possible participation of nitric oxide (NO), L-NAME (100 µM) was administered to aortic rings exposed to cumulatively increasing concentrations of PE in isolated aortic rings in the presence of the extract (10 µg/mL). Aqueous, butanol and dichloromethane fractions (10 µg/mL) obtained from the ethanol extract were assayed. Phytochemical screening was also performed. Results: Prazosin and A. bogotensis extract notably reduced the contraction induced by PE whereas their inhibitory effect in rings contracted with KCl were lower. A. bogotensis ethanol extract showed a high capacity for reducing the PE pressor response (pD´2: 5.51) as well as total efficacy for relaxing rings previously precontracted with PE. The relaxant efficacy and potency of A. bogotensis extract against rings previously contracted with KCl were notably lower. L-NAME partly reverted the inhibitory effect of A. bogotensis. Aqueous, butanol and dichloromethane fractions gave inhibitory responses lower than that obtained with the ethanol extract. Phytochemical screening of A. bogotensis extract revealed the significant presence of flavonoid and triterpene metabolites. Conclusions: These results suggest that A. bogotensis elicits a smooth muscle relaxant effect related to the alpha-1 antiadrenergic mechanism. This response is partially NO dependent and seems to be due to interactions among active metabolites likely to be of flavonoid and/or terpenoid nature.

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Tea, flavonoids, and cardiovascular health: endothelial protection

Cited by 89 publications

References 54 publications

Luteolinidin Protects the Postischemic Heart through CD38 Inhibition with Preservation of NAD(P)(H)

Luteolinidin Protects the Postischemic Heart through CD38 Inhibition with Preservation of NAD(P)(H)

Enhanced uptake and transport of (+)-catechin and (-)-epigallocatechin gallate in niosomal formulation by human intestinal Caco-2 cells

ALPHA ANTIADRENERGIC EFFECT OF Achyrocline bogotensis EXTRACT (“Vira Vira”) IN ISOLATED RAT AORTIC RING

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