Resveratrol protects myocardial ischemia–reperfusion injury through both NO-dependent and NO-independent mechanisms

Hung, Li-Man; Su, Ming‐Jai; Chen, Jan‐Kan

doi:10.1016/j.freeradbiomed.2003.12.016

Cited by 159 publications

(116 citation statements)

References 42 publications

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“…They have been shown to function as potent antioxidants and radical scavengers in vitro. Many studies have shown that increased dietary intake of flavonoid-rich foods decreases myocardial I/R injury in vivo (Hung et al, 2004;Ikizler et al, 2007;Toufektsian et al, 2008;Yamazaki et al, 2008), with many others showing protection by direct addition of flavonoids to the blood or perfusate in ex vivo isolated hearts (Amorini et al, 2003;Aneja et al, 2004;Fantinelli et al, 2005;Hirai et al, 2007;Scarabelli et al, 2009).…”

Section: Introductionmentioning

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: Introductionmentioning

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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“…It has been shown that pharmacological doses of RES exerts a regenerative affect on heart function in mice (79,80). As a result, RES has curative affect on myocardial function due to reduced free radical production (81,82) and increased antioxidant activity (83,84).…”

Section: Antioxidant Effect Of Res In Exercisementioning

confidence: 99%

Resveratrol and exercise

2016

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Abstract. Although it is recommended for a healthy lifestyle, moderate exercise is known to lead to oxidative stress, inflammation and muscle injury. Hence there are efforts to develop dietary strategies to counter the oxidative stress caused by physical activity. Recently, there has been an interest in the capability of resveratrol (RES) to modulate physical performance and prevent oxidative stress. Despite the inconsistency among reports regarding the topic, it has been suggested that RES delays fatigue by hindering lipid peroxidation. It is hypothesized that RES administration produces favorable effects on hepatic cell rejuvenation, exerts a regulatory effect on glucose metabolism, and preserves liver glycogen reserves that are diminished during physical activity. Consequently, there is a growing interest in the association between RES and exercise. The aim of the current review is to interpret the association between RES and exercise.

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“…It has been shown to possess diverse biochemical and physiological functions, including anti-aging (9), anti-platelet aggregation (201,312), anti-inflammatory (268), cardioprotection (15,116,119), and estrogenic properties (160). Experimental results from animal models have revealed that the anti-inflammatory properties of resveratrol control the development of arthritis (66), pancreatitis (198,199), and colitis (153).…”

Section: The Inhibitory Mechanisms Of Natural Compounds Against Npc Smentioning

confidence: 99%

Potential Therapeutic Molecular Targets for Nasopharyngeal Carcinoma

Chen¹

2012

Carcinogenesis, Diagnosis, and Molecular Targeted Treatment for Nasopharyngeal Carcinoma

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Resveratrol protects myocardial ischemia–reperfusion injury through both NO-dependent and NO-independent mechanisms

Cited by 159 publications

References 42 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)

Resveratrol and exercise

Potential Therapeutic Molecular Targets for Nasopharyngeal Carcinoma

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