Comparative study of the quercetin, ascorbic acid, glutathione and superoxide dismutase for nitric oxide protecting effects in mouse gastric fundus

Ertuğ, Peyman U.; Aydinoglu, Fatma; Öztürk, Özlem Görüroğlu; Şingirik, Ergin; Ogulener, Nuran

doi:10.1016/j.ejphar.2012.10.009

Cited by 21 publications

(12 citation statements)

References 52 publications

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“…Quercetin (3,3′,4′,5,7‐pentahydroxyflavone), an important dietary flavonoid present in several fruits and vegetables, exhibits antioxidant, anti‐inflammatory and anti‐cancer properties (Gibellini et al ., ). Quercetin scavenges superoxide anion, singlet oxygen and lipid peroxy radicals (Morales et al ., ; Ertuğ et al ., ) and inhibits copper‐catalysed oxidation (Filipe et al ., ). Several reports demonstrate that quercetin scavenges ROS and inhibits the activation of ERK and MAP kinase in ROS‐induced cardiomyopathy (Kyaw et al ., ; Angeloni et al ., ).…”

Section: Introductionmentioning

confidence: 99%

Quercetin attenuates doxorubicin cardiotoxicity by modulating Bmi‐1 expression

Dong

Chen

et al. 2014

British J Pharmacology

122

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Background and Purpose Doxorubicin‐based chemotherapy induces cardiotoxicity, which limits its clinical application. We previously reported the protective effects of quercetin against doxorubicin‐induced hepatotoxicity. In this study, we tested the effects of quercetin on the expression of Bmi‐1, a protein regulating mitochondrial function and ROS generation, as a mechanism underlying quercetin‐mediated protection against doxorubicin‐induced cardiotoxicity. Experimental Approach Effects of quercetin on doxorubicin‐induced cardiotoxicity was evaluated using H9c2 cardiomyocytes and C57BL/6 mice. Changes in apoptosis, mitochondrial function, oxidative stress and related signalling were evaluated in H9c2 cells. Cardiac function, serum enzyme activity and reactive oxygen species (ROS) generation were measured in mice after a single injection of doxorubicin with or without quercetin pre‐treatment. Key Results In H9c2 cells, quercetin reduced doxorubicin‐induced apoptosis, mitochondrial dysfunction, ROS generation and DNA double‐strand breaks. The quercetin‐mediated protection against doxorubicin toxicity was characterized by decreased expression of Bid, p53 and oxidase (p47 and Nox1) and by increased expression of Bcl‐2 and Bmi‐1. Bmi‐1 siRNA abolished the protective effect of quercetin against doxorubicin‐induced toxicity in H9c2 cells. Furthermore, quercetin protected mice from doxorubicin‐induced cardiac dysfunction that was accompanied by reduced ROS levels and lipid peroxidation, but enhanced the expression of Bmi‐1 and anti‐oxidative superoxide dismutase. Conclusions and Implications Our results demonstrate that quercetin decreased doxorubicin‐induced cardiotoxicity in vitro and in vivo by reducing oxidative stress by up‐regulation of Bmi‐1 expression. The findings presented in this study have potential applications in preventing doxorubicin‐induced cardiomyopathy.

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Section: Introductionmentioning

confidence: 99%

Quercetin attenuates doxorubicin cardiotoxicity by modulating Bmi‐1 expression

Dong

Chen

et al. 2014

British J Pharmacology

122

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“…Cardiovascular epidemiological studies showed that a population with a higher dietary intake of quercetin via tea, wine, fruits, vegetables, or other foods has lower incidence and decreased mortality of cardiovascular diseases [2][3][4]. Quercetin has been reported to possess a broad range of biological activities including antioxidant effects [5][6][7][8], antiplatelet aggregation [9], anti-inflammation [10], radioprotection [11], immunomodulation [12], improvement of lipid metabolism [13,14], antidiabetic properties [15], anticancer activities [16], and an improvement of human endurance exercise capacity [17]. Cardiovascular experimental studies showed that quercetin-supplemented diets lowered blood pressure and attenuated cardiac hypertrophy in rats with aortic constriction [18].…”

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confidence: 99%

Enhancement of Voltage-Gated K+ Channels and Depression of Voltage-Gated Ca2+ Channels Are Involved in Quercetin-Induced Vasorelaxation in Rat Coronary Artery

et al. 2014

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Quercetin is one of the most common flavonoids in the human daily diet. Its affects the coronary artery, especially L-type voltage-gated Ca2+ channels and voltage-gated K+ channels in the arterial smooth muscle cells, which are poorly understood. The present experiments were designed to study the myogenic effect of quercetin and its possible underlying mechanisms in the rat coronary artery. A wire myograph was used to observe the myogenic effects. Arterial smooth muscle cells were freshly isolated from the rat coronary artery and the intracellular free Ca2+ concentration was measured with molecular probe fluo-4-AM. The effects of quercetin on L-type voltage-gated Ca2+ channels and voltage-gated K+ channels were studied using a whole-cell patch clamp. Quercetin (3-30 µM) produced a depression and relaxation on the contraction induced by KCl or the thromboxane A2 analog 9,11-Dideoxy-9α,11α-methanoepoxy prostaglandin F 2α . The vasorelaxation was attenuated by 4-aminopyridine, a specific voltage-gated K+ channel inhibitor, but was not affected by the NG-nitro-L-arginine methylester ester (a nitric oxide synthesis inhibitor), glibenclamide (a ATP-activated K+ channel inhibitor), iberiotoxin (a Ca2+-activated K+ channel inhibitor), BaCl2 (an inward rectifier K+ channel inhibitor), or by endothelium denudation. At the same concentrations, quercetin reduced the KCl-induced elevation of the intracellular free Ca2+ concentration, inhibited the inward Ca2+ currents through L-type voltage-gated Ca2+ channels, and increased the outward K+ currents through voltage-gated K+ channels in the rat coronary artery smooth muscle cells. Collectively, our results demonstrate that quercetin possesses vasospasmolytic effects in RCA and suggest that depression of the Ca2+ influx through L-type voltage-gated Ca2+ channels and augmentation of voltage-gated K+ channel activity in the myocytes may underlie coronary relaxation.

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“…Quercetin has a variety of activities in man. For example, it has been reported to have antioxidant [5][6][7], anti-inflammatory [8], anti-anaphylactic [9], anti-aging [10], antiplatelet aggregatory [11], radioprotective [12], immunomodulatory [13], antidiabetic [14], and anticancer [15] effects, and to improve lipid metabolism [16,17] and endurance exercise capacity [18]. Quercetin also reduces gastrointestinal (GI) intestinal transit in mice [19], induces intestinal smooth muscle relaxation [20], and prevents castor oil-induced diarrhea [21].…”

Section: Introductionmentioning

confidence: 99%

Quercetin Inhibits Pacemaker Potentials via Nitric Oxide/cGMP-Dependent Activation and TRPM7/ANO1 Channels in Cultured Interstitial Cells of Cajal from Mouse Small Intestine

Gim¹,

Nam

Lee³

et al. 2015

Cell Physiol Biochem

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Background: Quercetin regulates gastrointestinal (GI) motor activity but the molecular mechanism involved has not been determined. The authors investigated the effects of quercetin, a flavonoid present in various foods, on the pacemaker activities of interstitial cells of Cajal (ICCs) in murine small intestine in vitro and on GI motility in vivo. Materials and Methods: Enzymatic digestion was used to dissociate ICCs from mouse small intestines. The whole-cell patch-clamp configuration was used to record pacemaker potentials in cultured ICCs in the absence or presence of quercetin and to record membrane currents of transient receptor potential melastatin (TRPM) 7 or transmembrane protein 16A (Tmem16A, anoctamin1 (ANO1)) overexpressed in human embryonic kidney (HEK) 293 cells. The in vivo effects of quercetin on GI motility were investigated by measuring the intestinal transit rates (ITRs) of Evans blue in normal mice. Results: Quercetin (100-200 μM) decreased the amplitudes and frequencies of pacemaker activity in a concentration-dependent manner in current clamp mode, but this action was blocked by naloxone (a pan-opioid receptor antagonist) and by GDPβS (a GTP-binding protein inhibitor). However, potassium channels were not involved in these inhibitory effects of quercetin. To study the quercetin signaling pathway, we examined the effects of 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), an inhibitor of guanylate cyclase, and of RP-8-CPT-cGMPS, an inhibitor of protein kinase G (PKG). These inhibitors blocked the inhibitory effects of quercetin on pacemaker activities. Also, L-NAME (100 μM), a non-selective NO synthase (NOS) inhibitor, blocked the effects of quercetin on pacemaker activity and quercetin stimulated cGMP production. Furthermore, quercetin inhibited both Ca²⁺-activated Cl^- channels (TMEM16A, ANO1) and TRPM7 channels. In vivo, quercetin (10-100 mg/kg, p.o.) decreased ITRs in normal mice in a dose-dependent manner. Conclusions: Quercetin inhibited ICC pacemaker activities by inhibiting TRPM7 and ANO1 via opioid receptor signaling pathways in cultured murine ICCs. The study shows quercetin attenuates GI tract motility, and suggests quercetin be considered the basis for the development of novel spasmolytic agents for the prevention or alleviation of GI motility dysfunctions.

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Comparative study of the quercetin, ascorbic acid, glutathione and superoxide dismutase for nitric oxide protecting effects in mouse gastric fundus

Cited by 21 publications

References 52 publications

Quercetin attenuates doxorubicin cardiotoxicity by modulating Bmi‐1 expression

Quercetin attenuates doxorubicin cardiotoxicity by modulating Bmi‐1 expression

Enhancement of Voltage-Gated K+ Channels and Depression of Voltage-Gated Ca2+ Channels Are Involved in Quercetin-Induced Vasorelaxation in Rat Coronary Artery

Quercetin Inhibits Pacemaker Potentials via Nitric Oxide/cGMP-Dependent Activation and TRPM7/ANO1 Channels in Cultured Interstitial Cells of Cajal from Mouse Small Intestine

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