Caffeinated coffee, decaffeinated coffee, and the phenolic phytochemical chlorogenic acid up-regulate NQO1 expression and prevent H2O2-induced apoptosis in primary cortical neurons

Kim, Jiyoung; Lee, Siyoung; Shim, Jaesung; Kim, Hyo Won; Kim, Jaekyoon; Jang, Young Jin; Yang, Hee Seok; Park, Ji‐Man; Choi, Seung Hwan; Yoon, Ji Hye; Lee, Ki Won; Lee, Hyong Joo

doi:10.1016/j.neuint.2012.02.004

Cited by 116 publications

(79 citation statements)

References 45 publications

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“…The chlorogenic acid (ChA), which is 45.1% of the total phenol content in APE has been shown to have multiple biological effects, including antioxidant (Feng et al, 2005), neuroprotective (Lee et al, 2008;Kwon et al, 2010) and neurotrophic activity (Ito et al, 2008). In H 2 O 2 -induced oxidative neuronal death, ChA up-regulated the antioxidant enzyme and the anti-apoptotic proteins, which probably exerted a neuroprotective effect on this population of neurons (Kim et al, 2012). In Verzelloni' (2011) study, low molecular-weight colonic catabolites of dietary polyphenols, that pass through the circulatory system before being excreted in urine, were shown to protect cultured neuroblastoma cells against mild oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

Protective effect of apple (Ralls) polyphenol extract against aluminum-induced cognitive impairment and oxidative damage in rat

Cheng

Cao

et al. 2014

NeuroToxicology

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Section: Discussionmentioning

confidence: 99%

Protective effect of apple (Ralls) polyphenol extract against aluminum-induced cognitive impairment and oxidative damage in rat

Cheng

Cao

et al. 2014

NeuroToxicology

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“…Carnosic acid was described by the same group to activate the Nrf2 pathway in both neurons and astrocytes and exhibit protection against focal ischemia/reperfusion brain injury [81]. Interestingly, chlorogenic acid, a compound found in both caffeinated and decaffeinated coffee, increases NQO1 expression in primary embryonic neurons without induction of other prototypical Nrf2-responsive genes such as heme oxygenase-1 [82]. …”

Section: Idebenone and Combination Therapy: Wave Of The Future?mentioning

confidence: 99%

“…Nrf2-dependent gene expression can be activated by small molecule electrophiles, including sulforaphane (SFP) or tert -butylhydroquinone (tBHQ) in astrocytes, by carnosic acid in both astrocytes and neurons, and by NEPP11 in neurons. Chlorogenic acid may induce neuronal NQO1 expression by Nrf2-independent mechanisms [82], although this has yet to be firmly established…”

Section: Figmentioning

confidence: 99%

Idebenone and neuroprotection: antioxidant, pro-oxidant, or electron carrier?

Jaber

Polster

2014

J Bioenerg Biomembr

108

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Ubiquinone, commonly called coenzyme Q10 (CoQ), is a lipophilic electron carrier and endogenous antioxidant found in all cellular membranes. In the mitochondrial inner membrane it transfers electrons to complex III of the electron transport chain. The short chain CoQ analogue idebenone is in clinical trials for a number of diseases that exhibit a mitochondrial etiology. Nevertheless, evidence that idebenone ameliorates neurological symptoms in human disease is inconsistent. Although championed as an antioxidant, idebenone can also act as a pro-oxidant by forming an unstable semiquinone at complex I. The antioxidant function of idebenone is critically dependent on two-electron reduction to idebenol without the creation of unstable intermediates. Recently, cytoplasmic NAD(P)H:quinone oxidoreductase 1 (NQO1) was identified as a major enzyme catalyzing idebenone reduction. While reduction allows idebenone to act as an antioxidant, evidence also suggests that NQO1 enables idebenone to shuttle reducing equivalents from cytoplasmic NAD(P)H to mitochondrial complex III, bypassing any upstream damage to the electron transport chain. In this mini-review we discuss how idebenone can influence mitochondrial function within the context of cytoprotection. Importantly, in the brain NQO1 is expressed primarily by glia rather than neurons. As NQO1 is an inducible enzyme regulated by oxidative stress and the nuclear factor erythroid 2-related factor 2 (Nrf2)/antioxidant response element (ARE) pathway, optimizing NQO1 expression in appropriate cell types within a specific disease context may be key to delivering on idebenone's therapeutic potential.

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“…Alternatively, the activation of phosphatases, which may regulate TrkB autophosphorylation negatively [24], is another possible mechanism for the coffee-induced reduction of TrkB phosphorylation. Surprisingly, the major constituents of coffee (caffeine, caffeic acid, chlorogenic acid, and trigonelline) did not have any significant effect on BDNF/TrkB signaling in SH-SY5Y cells, although recent studies proposed that caffeine, chlorogenic acid, and trigonelline might be neuroprotective [12] [25] [26]. Further studies to identify the active compounds in coffee are warranted to clarify the inhibitory mechanism of coffee on TrkB phosphorylation in the cells.…”

Section: Discussionmentioning

confidence: 99%

Coffee Modulates the Function of Brain-Derived Neurotrophic Factor (BDNF) in Human Neuroblastoma SH-SY5Y Cells

Kakio¹,

Nakazawa²,

Funakoshi‐Tago³

et al. 2015

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Recent epidemiological studies showed that daily coffee consumption is associated with a lower risk for several neurological disorders such as Alzheimer's disease and Parkinson's disease; however, the molecular mechanisms responsible for the protective effect of coffee against neurological disorders have not been elucidated. As brain-derived neurotrophic factor (BDNF) promotes neuronal survival and protects against neuronal damage, we investigated the effects of coffee on BDNF signaling using human neuroblastoma SH-SY5Y cells. We found that brewed coffee exerted an inhibitory effect on the autophosphorylation of tropomyosin receptor kinase B (TrkB), a BDNF receptor. Additionally, coffee reduced the phosphorylation of Akt in BDNF-treated SH-SY5Y cells. Treatment with coffee did not affect the TrkB receptor on the cell surface. The major constituents of coffee, such as caffeine, caffeic acid, chlorogenic acid, and trigonelline had no effect on TrkB phosphorylation induced by BDNF. In addition, coffee reduced the BDNF-induced increase in BDNF gene expression and the neurite outgrowth promoted by BDNF. Our data suggest that the protective effect of coffee reported in epidemiological studies against neurological disorders may not be associated with BDNF signaling through TrkB.

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Caffeinated coffee, decaffeinated coffee, and the phenolic phytochemical chlorogenic acid up-regulate NQO1 expression and prevent H2O2-induced apoptosis in primary cortical neurons

Cited by 116 publications

References 45 publications

Protective effect of apple (Ralls) polyphenol extract against aluminum-induced cognitive impairment and oxidative damage in rat

Protective effect of apple (Ralls) polyphenol extract against aluminum-induced cognitive impairment and oxidative damage in rat

Idebenone and neuroprotection: antioxidant, pro-oxidant, or electron carrier?

Coffee Modulates the Function of Brain-Derived Neurotrophic Factor (BDNF) in Human Neuroblastoma SH-SY5Y Cells

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