Corrigendum to Flavonoid permeability across an in situ model of the blood–brain barrier. Free Radic. Biol. Med. 36: 592–604; 2004.

Youdim, Kuresh A.; Qaiser, M. Zeeshan; Begley, David J.; Rice‐Evans, Catherine; Abbott, N. Joan

doi:10.1016/j.freeradbiomed.2004.03.003

Cited by 24 publications

(9 citation statements)

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“…Using an in vitro model of BBB, a recent study reported measurable permeabilities for naringenin, quercetin and their in vivo glucuronidated conjugates across the BBB model, which were consistent with their lipophilicity properties [22], as well as for the anthocyanins cyanidine-3-rutinoside, pelargonidin-3-glucoside, epicatechin and hydroxycinnamates [23]. In line with these observations, other investigators identified narigenin and its glucuronide conjugate in several regions of rat brain following i.v.…”

Section: Bioavailability Of Polyphenolssupporting

confidence: 54%

Mechanisms of Neuroprotection by Polyphenols

Frade

Ferreira

Barbosa

et al. 2005

CMCCNSA

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Several lines of evidence suggest a role for oxidative cascades of events leading to neurodegeneration associated with Parkinson's, Alzheimer, Huntington diseases, and amyotrophic lateral sclerosis. In agreement with the notion of oxidative/nitrosative involvement in these chronic diseases, in vivo models of disease as well as biochemical and epidemiological evidence suggest a neuroprotective role for natural antioxidant polyphenols in neurodegenerative diseases. However, the molecular mechanisms for neuroprotection do not merely rely on a direct radical scavenging/antioxidant activity. Rather, polyphenols may function at several cellular levels, including direct interaction and modulation of enzymatic activities and the regulation of signaling pathways with implications for cell survival and death. Nitric oxide is a paradigmatic example. In view of the wide collection of activities of nitric oxide in the brain, ranging from synaptic plasticity to excitotoxicity, the regulation of its rate and pattern of production and decay in tissues by polyphenols is of obvious physiological relevance. Thus, the elucidation of polyphenol activities at the molecular level may lay the foundations for new pharmacological approaches in relation to neurodegeneration. In this review, the molecular mechanisms underlying the potential health promoting effects of natural polyphenols in connection with neurodegenerative diseases are discussed. Additionally, we provide evidence for a modulatory effect of hydroxycinnamic phenol caffeic acid on glutamate NMDA receptor/nitric oxide pathway in hippocampal slices.

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Section: Bioavailability Of Polyphenolssupporting

confidence: 54%

Mechanisms of Neuroprotection by Polyphenols

Frade

Ferreira

Barbosa

et al. 2005

CMCCNSA

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“…27 At present, we are not able to hypothesize a precise mechanism for this behaviour. We can only suggest two possible explanations for the significant accumulation of quercetin in the brain in the presence of α-tocopherol: (i) the ability of α-tocopherol to inhibit P-glycoprotein, 48,49 a membrane glycoprotein, extensively distributed in neurons and astrocytes, which allows the efflux of xenobiotics out of the cell; 49 (ii) the ability of α-tocopherol to inhibit protein kinase C (PKC) by means of protein phosphatase 2A activation, 50 thus impairing the phosphorylation/dephosphorylation mechanism in quercetin transport across the BBB, which controls the in/out flux of metabolites. 29,50 The two mechanisms could also work together.…”

Section: Resultsmentioning

confidence: 98%

Enhancement of flavonoid ability to cross the blood–brain barrier of rats by co-administration with α-tocopherol

et al. 2015

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Vitamin E and polyphenols could exhibit a therapeutic role in the treatment of oxidative stress-induced neurodegenerative diseases. Therefore, their ability to cross the blood-brain barrier (BBB) represents an important issue to be explored by different diet combinations. In this study, we have evaluated the ability of α-tocopherol to support epigallocatechin-3-gallate (EGCG), quercetin and rutin to cross the BBB, following oral administration. Eighteen rats were fed a standard diet (C), a diet supplemented with α-tocopherol (A), with a mixture of EGCG, quercetin and rutin (P); or with a mixture of α-tocopherol and the three flavonoids (AP). Flavonoids and their conjugated derivatives were assayed in brain and plasma by HPLC-MS, whereas α-tocopherol was detected by RP-HPLC. The oxidative damage, due to the potential pro-oxidant activity of flavonoids, was evaluated by the presence of 8-hydroxy-2'-deoxyguanosine (8-OHdG) in hippocampal Cornus Ammonis, one of the most vulnerable sites in the brain. Our results indicate that α-tocopherol is able to promote quercetin transport across the BBB. The mixture of rutin and quercetin seems to favour the accumulation of quercetin and/or its conjugated derivatives in the brain. In contrast, α-tocopherol does not affect EGCG transport across the BBB. The densitometric analysis of 8-OHdG immunoreactivity does not reveal any difference of oxidative damage among the experimental groups. Our results suggest that α-tocopherol may promote quercetin transport across the BBB, leading to a significant increase of α-tocopherol and quercetin concentration in the brain.

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“…Transportation of these metabolites into the brain tissues via the blood brain barrier and their effect on the CNS system have been recently argued. 32,33) Moreover, quercetin metabolites were previously found in the brain tissues of rodents after oral administration. 34) Therefore, one of the antidepressant mechanisms of EGB is thought to involve flavonoid glycosides, which reach the brain tissues through the metabolizing process, protecting brain function from CNS disturbance, and consequently, exerting an antidepressant effect.…”

Section: Discussionmentioning

confidence: 99%

Antidepressant Effect of Extracts from Ginkgo biloba Leaves in Behavioral Models

Sakakibara

Ishida

Grundmann

et al. 2006

Biological & Pharmaceutical Bulletin

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In recent years, depression has become recognized as a major public health problem. It is estimated that in the US approximately 20% of the population has some depressive symptoms, and around 2-5% are thought to suffer from severe forms of depression.1) Understanding how to prevent and treat depression is therefore an urgent subject. Although the mechanism provoking depression has not been clearly elucidated, the main trigger is known to be exposure to chronic stress.2,3) Many types of antidepressant drugs such as tricyclic antidepressants, and selective serotonin reuptake inhibitors (SSRI), as well as antidepressant herbal medicines like St. John's wort are used to treat depression. However, most of the synthetic drugs are not without side effects. 4)Furthermore disturbance of the drug metabolizing enzyme systems were revealed with St. John's wort, 5) and thus, the search for a new antidepressant herb without side effects is deemed important.The Ginkgo biloba tree has been used as a traditional Chinese herbal medicine for thousands of years.6) Several research groups have shown that extracts from the green leaves of the G. biloba tree (EGB) have diverse effects on improvement of mood and cognitive performance, protection of memory deficits and central nervous system (CNS) disorders, and alleviation of the symptoms of mild to moderate Alzheimer-type dementia.7-12) Until now, no antidepressant effect of EGB has yet been revealed. EGB is thought to possess anti-stress properties, 13) and is safe to use without distinct side effects. 8,14) EGB might be a useful option for the prevention and treatment for stress-induced disorders such as depression. In the present study, we evaluated the antidepressant effect of EGB using two behavioral models for screening antidepressants, the forced swimming test (FST) in rats and tail suspension test (TST) in mice. MATERIALS AND METHODS ChemicalsThe EGB used in the present study was Ginkgolon-24 from Tokiwa Phytochemical Co., Ltd. (Chiba, Japan), which was 75% ethanol extracts from the leaves of Japanese G. biloba tree. This product contains 25.5% of flavonoid glycosides, including more than 8.2% quercetin glycosides, more than 6.4% kaempferol glycosides, 1.6% methylmyricetin glycosides and 1.3% isorhamnetin glycosides, and 6.5% of terpenoids in the form of 2.98% bilobalide, 1.59% ginkgolide A, 1.16% ginkgolide B, and 0.75% ginkgolide C. The antidepressant drug imipramine (hydrochloride form) was purchased from Sigma-Aldrich Co. (St. Louis, MO, U.S.A.).Animals Male CD rats (240-260 g; Charles River Japan, Inc., Yokohama, Japan) and male C57BL/6J mice (22-26 g; SLC, Inc., Hamamatsu, Japan) were used in the FST and TST, respectively. All animals were housed in a controlled room (temperature, 25Ϯ1°C; humidity, 45-50%; light-dark cycle, 12 h each) with free access to laboratory chow (MF; Oriental Yeast Co., Ltd., Tokyo, Japan) and tap water. Rodents were divided randomly into control and experimental groups. This study was performed according to the guidelines for the care and use of...

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Corrigendum to Flavonoid permeability across an in situ model of the blood–brain barrier. Free Radic. Biol. Med. 36: 592–604; 2004.

Cited by 24 publications

References 0 publications

Mechanisms of Neuroprotection by Polyphenols

Mechanisms of Neuroprotection by Polyphenols

Enhancement of flavonoid ability to cross the blood–brain barrier of rats by co-administration with α-tocopherol

Antidepressant Effect of Extracts from Ginkgo biloba Leaves in Behavioral Models

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