Anti-apoptotic effect of quercetin: Intervention in the JNK- and ERK-mediated apoptotic pathways

Ishikawa, Yoshihiro; Kitamura, Masanori

doi:10.1046/j.1523-1755.2000.00265.x

Cited by 197 publications

(95 citation statements)

References 40 publications

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“…The flavanols, epicatechin and 3 0 -O-methyl-epicatechin have been shown to protect neurons against oxidative damage via a mechanism involving the suppression of JNK, and downstream partners, c-jun and pro-caspase-3 [149,161]. In support of these observations, the flavone, baicalein, has been shown to significantly inhibit 6-OHDAinduced JNK activation and neuronal cell death and quercetin may suppress JNK activity and apoptosis induced by hydrogen peroxide [78,181], 4-hydroxy-2-nonenal [173] and tumour necrosis factor-alpha (TNF-alpha) [92]. There are a number of potential sites where flavonoids may interact with the JNK pathway.…”

Section: Stress-activated Protein Kinases: C-jun-n-terminal Kinase (Jmentioning

confidence: 81%

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: Stress-activated Protein Kinases: C-jun-n-terminal Kinase (Jmentioning

confidence: 81%

The interactions of flavonoids within neuronal signalling pathways

2007

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“…The activa- tion of ERK was suggested to be a critical components in the oxidative stress induced apoptosis process. 40) Activated ERK can induce c-Fos, which is a component of AP-1. 41) Previous studies have demonstrated that AP-1 is an important regulator of proliferation, transformation, and apoptosis, depending on the cell type.…”

Section: Discussionmentioning

confidence: 99%

Cytoprotective Effects of KIOM-79 on Streptozotocin Induced Cell Damage by Inhibiting ERK and AP-1

Kang

Lee

Kim

et al. 2007

Biological & Pharmaceutical Bulletin

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“…However, other studies using different model systems have produced findings to suggest that ERK activation can contribute to apoptosis in response to oxidant injury. These include hyperoxiainduced apoptosis of macrophages (Petrache et al, 1999), cisplatin-induced apoptosis of HeLa cells , hydrogen peroxide-induced apoptosis of oligodendrocytes (Bhat and Zhang, 1999;Brand et al, 2001) and mesengial cells (Ishikawa and Kitamura, 2000), and asbestos-induced apoptosis of pleural mesothelial cells (Jimenez et al, 1997). What determines whether ERK will act in a pro-apoptotic or anti-apoptotic fashion remains an important unanswered question, but the kinetics and duration of its activation may be important factors.…”

Section: Erk Pathwaymentioning

confidence: 99%

Cellular response to oxidative stress: Signaling for suicide and survival*

Martindale

Holbrook

2002

Journal Cellular Physiology

2,059

1,569

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Reactive oxygen species (ROS), whether produced endogenously as a consequence of normal cell functions or derived from external sources, pose a constant threat to cells living in an aerobic environment as they can result in severe damage to DNA, protein, and lipids. The importance of oxidative damage to the pathogenesis of many diseases as well as to degenerative processes of aging has becoming increasingly apparent over the past few years. Cells contain a number of antioxidant defenses to minimize fluctuations in ROS, but ROS generation often exceeds the cell's antioxidant capacity, resulting in a condition termed oxidative stress. Host survival depends upon the ability of cells and tissues to adapt to or resist the stress, and repair or remove damaged molecules or cells. Numerous stress response mechanisms have evolved for these purposes, and they are rapidly activated in response to oxidative insults. Some of the pathways are preferentially linked to enhanced survival, while others are more frequently associated with cell death. Still others have been implicated in both extremes depending on the particular circumstances. In this review, we discuss the various signaling pathways known to be activated in response to oxidative stress in mammalian cells, the mechanisms leading to their activation, and their roles in influencing cell survival. These pathways constitute important avenues for therapeutic interventions aimed at limiting oxidative damage or attenuating its sequelae. Published 2002 Wiley‐Liss, Inc.

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Anti-apoptotic effect of quercetin: Intervention in the JNK- and ERK-mediated apoptotic pathways

Abstract: These results suggested that (1) activation of JNK and ERKs, but not p38 kinase, is required for the H2O2-induced apoptosis; and (2) suppression of the JNK-c-Jun/AP-1 pathway and the ERK-c-Fos/AP-1 pathway is involved in the anti-apoptotic effect of quercetin.

Cited by 197 publications

References 40 publications

The interactions of flavonoids within neuronal signalling pathways

The interactions of flavonoids within neuronal signalling pathways

Cytoprotective Effects of KIOM-79 on Streptozotocin Induced Cell Damage by Inhibiting ERK and AP-1

Cellular response to oxidative stress: Signaling for suicide and survival*

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