Depolarization-dependent effect of flavonoids in rat uterine smooth muscle contraction elicited by CaCl2

Revuelta, Manuel; Cantabrana, Begoña; Hidalgo, Agustı́n

doi:10.1016/s0306-3623(97)00002-5

Cited by 96 publications

(72 citation statements)

References 52 publications

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“…Flavonoids have the potential to bind to the ATP-binding sites of a large number of proteins [38] including, mitochondrial ATPase [50], calcium plasma membrane ATPase [13], protein kinase A [136], protein kinase C [61,81,101,142,176] and topoisomerase [18]. In addition, interactions with the benzodiazepine binding sites of GABA-A receptors and with adenosine receptors [48,117] have been reported.…”

Section: Flavonoid Interactions With Neuronal Signalling Cascadesmentioning

confidence: 99%

The interactions of flavonoids within neuronal signalling pathways

2007

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Emerging evidence suggests that dietary phytochemicals, in particular flavonoids, may exert beneficial effects in the central nervous system by protecting neurons against stress-induced injury, by suppressing neuroinflammation and by promoting neurocognitive performance, through changes in synaptic plasticity. It is likely that flavonoids exert such effects in neurons, through selective actions on different components within a number of protein kinase and lipid kinase signalling cascades, such as phosphatidylinositol-3 kinase (PI3K)/Akt, protein kinase C and mitogen-activated protein kinase. This review details the potential inhibitory or stimulatory actions of flavonoids within these pathways, and describes how such interactions are likely to affect cellular function through changes in the activation state of target molecules and/or by modulating gene expression. Although, precise sites of action are presently unknown, their abilities to: (1) bind to ATP binding sites on enzymes and receptors; (2) modulate the activity of kinases directly; (3) affect the function of important phosphatases; (4) preserve neuronal Ca 2+ homeostasis; and (5) modulate signalling cascades lying downstream of kinases, are explored. Future research directions are outlined in relation to their precise site(s) of action within the signalling pathways and the sequence of events that allow them to regulate neuronal function in the central nervous system.

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Section: Flavonoid Interactions With Neuronal Signalling Cascadesmentioning

confidence: 99%

The interactions of flavonoids within neuronal signalling pathways

2007

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“…Since flavonoids have been reported to bind to benzodiazepine binding sites of GABA-A and adenosine receptors [52,132], they might also exert an effect on the mPTP and, therefore, modulate cytochrome c release. In addition flavonoids have been found to bind to ATP-binding sites of proteins [43] such as the mitochondrial ATPase [53], calcium plasma membrane ATPase [10] protein kinase A [164], PKC [117] and topoisomerase [17] all of which must be considered in intracellular responses to oxidative insults. Thus, flavonoids might be able to modulate mitochondrial functions by binding to ATP binding sits on the ANT, ATPases or others.…”

Section: Flavonoids: Neuroprotective Agents In Vivo and In Vitro?mentioning

confidence: 99%

MAPK signaling in neurodegeneration: influences of flavonoids and of nitric oxide

Schroeter

Boyd

Spencer

et al. 2002

Neurobiology of Aging

302

178

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Oxidative and nitrosative stress is increasingly associated with the pathology of neurodegeneration and aging. The molecular mechanisms underlying oxidative/nitrosative stress-induced neuronal damage are emerging and appear to involve a mode of death in which mitogen-activated protein kinase (MAPK) signaling pathways are strongly implicated. Thus, attention is turning towards the modulation of intracellular signaling as a therapeutic approach against neurodegeneration. Both endogenous and dietary agents have been suggested as potent modulators of intracellular signal transduction, e.g. nitric oxide and flavonoids, respectively. This review addresses recent findings on the biological effects of flavonoids and nitric oxide in neurodegeneration and aims to elucidate the rationale for their prospective use as modulators of cellular signal transduction. © 2002 Elsevier Science Inc. All rights reserved.Keywords: Apoptosis; Oxidative stress; Neuron; Flavonoids; MAP kinase; JNK; ERK; Epicatechin; Nitric oxide; Mitochondria; Redox status; Polyphenols Abbreviations: AKT, serine/threonine kinase (also known as protein kinase B); AP-1, activator protein-1; Apaf-1, apoptosis protease activating factor-1; ASK1, apoptosis signal-regulating kinase-1; Bad, Bcl-2/BclX Lassociated death promoting protein; Bax, pro-apoptotic protein of the Bcl-2 family; Bcl-2, B-cell lymphoma 2: protein with anti-apoptotic properties; BclX L , long form of Bclx: anti-apoptotic protein of the Bcl-2 family; Caspase, cysteinyl aspartic acid-protease; c-Jun, mammalian equivalent of Jun: part of the AP-1 transcription complex; CREB, cAMP response element binding protein; DIABLO/smac, mitochondria-related pro-apoptotic protein: inhibits XIAP; ERK1/2, extracellular signal-related kinase; Fas, CD95: member of the TNF receptor family; GSHST, glutathione Stransferase; JNK, c-Jun amino-terminal kinase; MAPK, mitogen-activated protein kinase; MAPKK, MAPK kinase; MAPKKK, MAPKK kinase; MEK1/2, ERK1/2-specific MAPKK; MKK4/7, JNK-specific MAPKK; MSK1, mitogen-and stress-activated kinase-1; NF-B, nuclear factor of immunoglobulin k locus in B-cells; ONOO − , peroxynitrite anion; p53, pro-apoptotic tumor suppressor gene product; PI3-kinase, phosphoinositol 3-kinase; Ras, small G-protein; RNS, reactive nitrogen species; ROS, reactive oxygen species; RSK, pp90 ribosomal S6 kinase; SAPK, stressactivated protein kinase; XIAP, X-linked inhibitor of apoptosis: inhibits the activation of caspase-9

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“…In a study by Revuelta et al (1997), quercetin and kaemferol relaxed rat isolated uteri precontracted with potassium chloride. Thus, it is not unreasonable to speculate that quercetin, kaemferol and other flavonoids present in PGE might have contributed, at least in part, to the uterine relaxant effects observed in the present study.…”

Section: Discussionmentioning

confidence: 99%

“…However, the failure of propranolol to modify uterine relaxant effect of PGE strongly suggests that PGE-induced uterine relaxation is probably not mediated via β2-adrenoceptor activation. In a study by Revuelta et al, (1997), an inhibitor of cyclic adenosine monophosphate (cAMP)-dependent protein kinase (PKA) and protein kinase C (PKC), N-p-tosyl-1-phenylalanine-chloromethyl-ketone (TPCK), significantly antagonised the uterine relaxation elicited by quercetin and kaemferol; thus suggesting that quercetin and kaempferol increase intracellular cAMP. The elevated intracellular cAMP would thus appear to contribute towards the relaxation of the uterus.…”

Section: Discussionmentioning

confidence: 99%

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Spasmolytic effect of Psidium guajava Linn. (Myrtaceae) leaf aqueous extract on rat isolated uterine horns

Chiwororo

Ojewole

2009

J. Smooth Muscle Res.

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Globally, primary dysmenorrhoea is one of the most frequent gynaecological disorders in young women. It is associated with increased uterine tone, and exaggerated contractility of uterine smooth muscles. In many rural African communities, a number of medicinal plants, including Psidium guajava Linn. (family: Myrtaceae), are used traditionally for the management, control and/or treatment of primary dysmenorrhoea. The present study was, therefore, undertaken to examine the spasmolytic effect of Psidium guajava leaf aqueous extract (PGE) on isolated, spontaneously-contracting and oestrogen-dominated, quiescent uterine horns of healthy, young adult, female Wistar rats. Graded, escalated concentrations of PGE (0.5-4.0 mg/ml) produced concentration-dependent and significant inhibitions of the amplitude of spontaneous phasic contractions of the isolated rat uterine horn preparations. In a concentration-related manner, PGE also significantly inhibited or abolished contractions produced by acetylcholine (ACh, 0.5-8.0 µg/ml), oxytocin (0.5-4.0 µU), bradykinin (2.5-10 ng/ml), carbachol (CCh, 0.5-8.0 µg/ml) or potassium chloride (K + , 10-80 mM) in quiescent uterine horn preparations isolated from the oestrogendominated rats. The spasmolytic effect of PGE observed in the present study lends pharmacological support to the traditional use of 'guava' leaves in the management, control and/or treatment of primary dysmenorrhoea in some rural African communities.

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Depolarization-dependent effect of flavonoids in rat uterine smooth muscle contraction elicited by CaCl2

Cited by 96 publications

References 52 publications

The interactions of flavonoids within neuronal signalling pathways

The interactions of flavonoids within neuronal signalling pathways

MAPK signaling in neurodegeneration: influences of flavonoids and of nitric oxide

Spasmolytic effect of Psidium guajava Linn. (Myrtaceae) leaf aqueous extract on rat isolated uterine horns

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