Nitric Oxide (NO) Scavenging and NO Protecting Effects of Quercetin and Their Biological Significance in Vascular Smooth Muscle

López-López, Gustavo; Moreno, Laura; Cogolludo, Ángel; Galisteo, Milagros; Ibarra, Manuel; Duarte, Juan; Lodi, Federica; Tamargo, Juan; Pérez‐Vizcaíno, Francisco

doi:10.1124/mol.65.4.851

Cited by 88 publications

(78 citation statements)

References 32 publications

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“…Lopez-Lopez et al [16] reported that quercetin had the ability to reduce blood pressure and endothelial dysfunction in animal models of hypertension. The hypertension and oxidative stress prevention, and the vascular protection effects by chronic treatment of quercetin were also reported [17].…”

Section: Introductionmentioning

confidence: 99%

Regulation of polyphenols accumulation by combined overexpression/silencing key enzymes of phyenylpropanoid pathway

Chang¹,

Luo²,

He³

2009

ABBS

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There is a growing interest in the metabolic engineering of plant with increased desirable polyphenols such as chlorogenic acid (CGA) and rutin. In this study, the effects of overexpression of both phenylalanine ammonia lyase (AtPAL2), the first enzyme of the phenylpropanoid pathway, and hydroxycinnamoyl-CoA quinate:hydroxycinnamoyl transferase (NtHQT), the last enzyme of CGA biosynthesis, and the overexpression of AtPAL2 together with silencing of NtHQT were investigated in tobacco. Transgenic tobacco plants overexpressing AtPAL2 showed two and five times increases of CGA and rutin levels than the wild-type (WT) plants, respectively. Overexpression of NtHQT further increases the accumulation of CGA in the AtPAL2 plants to about three times than that of the WT level, while silencing of NtHQT in AtPAL2 plants results in 12 times increase in rutin level than that of the WT plants. Simultaneous overexpression of phenylalanine ammonia lyase (PAL) and overexpression/silencing HQT could be used for the production of functional food with increased polyphenols.

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Section: Introductionmentioning

confidence: 99%

Regulation of polyphenols accumulation by combined overexpression/silencing key enzymes of phyenylpropanoid pathway

Chang¹,

Luo²,

He³

2009

ABBS

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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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“…2-(4-Carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (c-PTIO) and the flavonoid quercetin are specific NO scavengers [170][171][172]; Uric acid and hesperetin are peroxynitrite scavengers [173,174]. These have been used for determination of RNS involvement as well.…”

Section: Methods To Evaluate the Involvement Of Ros And/or Rns In Phymentioning

confidence: 99%

Oxidative Stress and Neurodegenerative Disorders

Qureshi¹,

Parvez²

2007

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Living cells continually generate reactive oxygen species (ROS) through the respiratory chain during energetic metabolism. ROS at low or moderate concentration can play important physiological roles. However, an excessive amount of ROS under oxidative stress would be extremely deleterious. The central nervous system (CNS) is particularly vulnerable to oxidative stress due to its high oxygen consumption, weakly antioxidative systems and the terminal-differentiation characteristic of neurons. Thus, oxidative stress elicits various neurodegenerative diseases. In addition, chemotherapy could result in severe side effects on the CNS and peripheral nervous system (PNS) of cancer patients, and a growing body of evidence demonstrates the involvement of ROS in drug-induced neurotoxicities as well. Therefore, development of antioxidants as neuroprotective drugs is a potentially beneficial strategy for clinical therapy. In this review, we summarize the source, balance maintenance and physiologic functions of ROS, oxidative stress and its toxic mechanisms underlying a number of neurodegenerative diseases, and the possible involvement of ROS in chemotherapy-induced toxicity to the CNS and PNS. We ultimately assess the value for antioxidants as neuroprotective drugs and provide our comments on the unmet needs.

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Nitric Oxide (NO) Scavenging and NO Protecting Effects of Quercetin and Their Biological Significance in Vascular Smooth Muscle

Cited by 88 publications

References 32 publications

Regulation of polyphenols accumulation by combined overexpression/silencing key enzymes of phyenylpropanoid pathway

Regulation of polyphenols accumulation by combined overexpression/silencing key enzymes of phyenylpropanoid pathway

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

Oxidative Stress and Neurodegenerative Disorders

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