<i>Allium cepa</i> Extract and Quercetin Protect Neuronal Cells from Oxidative Stress via PKC‐<i>ε</i> Inactivation/ERK1/2 Activation

Lee, Bo Kyung; Jung, Yi‐Sook

doi:10.1155/2016/2495624

Cited by 31 publications

(22 citation statements)

References 34 publications

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“…In the last 20 years, there has been an explosion of studies on the neuroprotective effects of various fruits and vegetables due to their bioactive components, particularly the flavonoids (Magalingam et al, 2015b). Among vegetables the onion, Allium cepa, is rich in flavonoids and has been demonstrated to have neuroprotective proprieties mainly attributed to its principal flavonoid quercetin (Shri and Singh Bora, 2008;Singh and Goel, 2015;Yang et al, 2013;Lee and Jung, 2016).…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective effects of quercetin 4’- O -β- d -diglucoside on human striatal precursor cells in nutrient deprivation condition

et al. 2018

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Several investigations have demonstrated neuroprotective effects of quercetin, a polyphenol widely present in nature, against neurotoxic chemicals, as well as in neuronal injury/neurodegenerative disease models. Most of these studies have been performed with quercetin aglycone and its metabolites, while scanty data are available on its glycosides. This study is aimed at investigating the neuroprotective effects of quercetin 3,4'-O-β-d-diglucoside (Q3,4'dG), isolated from the bulbs of the white cultivar (Allium cepa L.), using an in vitro model of human striatal precursor cells (HSPs), a primary culture isolated from the striatal primordium and previously characterized. To study the effect of Q3,4'dG on cell survival, HSPs were exposed to nutrient deprivation created by replacing culture medium with phosphate buffer saline (PBS). Our findings showed that Q3,4'dG treatment significantly promoted cell survival and strongly decreased apoptosis induced by nutrient deprivation, as evaluated by cell proliferation/death analyses. In addition, since the adhesive capacities of cells are essential for cell survival, the expression of some adhesion molecules, such as pancadherin and focal adhesion kinase, was evaluated. Interestingly, PBS exposure significantly decreased the expression of both molecules, while in the presence of Q3,4'dG this effect was prevented. This study provides evidence of a neuroprotective role exerted by Q3,4'dG and suggests its possible implication in sustaining neuronal survival for prevention and treatment of neurodegenerative disorders.

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Section: Discussionmentioning

confidence: 99%

Neuroprotective effects of quercetin 4’- O -β- d -diglucoside on human striatal precursor cells in nutrient deprivation condition

et al. 2018

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“… 41 In previous studies, Qu has been shown to have both inhibitory and promoting effects on ERK1/2, possibly depending on cell and tissue type. 42 - 44 The effect of Qu on AMPK signaling is positive in various cells. Qu augments AMPK signaling, blocking the AKT/mTOR cascades and reducing breast cancer growth and metastasis in nude mice.…”

Section: Discussionmentioning

confidence: 99%

Quercetin Has Antimetastatic Effects on Gastric Cancer Cells via the Interruption of uPA/uPAR Function by Modulating NF-κb, PKC-δ, ERK1/2, and AMPKα

Chen

2017

Integr Cancer Ther

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Gastric cancer (GC) is a malignancy with few effective treatment options after metastasis occurs. Quercetin (Qu) intake has been associated with reduced incidence and slow development of GC, probably due to its anti-proliferative and apoptotic effects, but it is unclear whether Qu can inhibit the metastatic activity. The urokinase plasminogen activator (uPA)/uPA receptor (uPAR) system plays an important role in cancer metastasis. In this study, we measured both uPA activity and uPAR expression in GC and pericarcinous tissues, and we investigated the correlation between uPAR expression and the migratory and invasive activities of various GC cell lines. GC BGC823 and AGS cells were subjected to treatment with 10 μM Qu for 72 hours and uPAR knockdown, alone or in combination, before evaluating cell metastasis. The results showed that uPA activity and uPAR expression were higher in GC tissues than in pericarcinous tissues. Migratory and invasive activities of GC cell lines positively correlated with uPAR expression. Qu treatment decreased BGC823 and AGS cell migration and invasion, accompanied by reduced uPA and uPAR protein expression. Both Qu treatment and uPAR knockdown decreased matrix metalloproteinase-2 and -9 activity and blocked Pak1-Limk1-cofilin signaling. Qu treatment was associated with inhibition of NF-κb, PKC-δ, and ERK1/2, and with AMPKα activation. Specific inhibitors of NF-κb, PKC, and ERK1/2, and an AMPKα activator suppressed uPA and uPAR expression in GC cells. Collectively, Qu showed an antimetastatic effect on GC cells via the interruption of uPA/uPAR function and modulation of NF-κb, PKC-δ, ERK1/2, and AMPKα. This suggests that Qu is a promising agent against GC metastasis.

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“…Moreover, quercetin treatment reverses impaired autophagic activity and results in the protection of the brain against oxidative stress [186]. Furthermore, quercetin reduces PKCε/p38MAPK mediated ROS production through the activation of the ERK1/2 pathway to protect neurons from oxidative stress [187] and it is indicated that GSK-β and p38 inhibition or PKC activation results in Nrf2 phosphorylation under quercetin treatment [188]. Suppression of PKCε and TRPV1 in the spinal cord by quercetin has the potential for the treatment of acute neuropathic pain [189].…”

Section: Polyphenols Act As Neuroprotective Agent During Pkc and Automentioning

confidence: 99%

Protein Kinase C Isozymes and Autophagy during Neurodegenerative Disease Progression

Kaleli

Özer

Kaya

et al. 2020

Cells

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Protein kinase C (PKC) isozymes are members of the Serine/Threonine kinase family regulating cellular events following activation of membrane bound phospholipids. The breakdown of the downstream signaling pathways of PKC relates to several disease pathogeneses particularly neurodegeneration. PKC isozymes play a critical role in cell death and survival mechanisms, as well as autophagy. Numerous studies have reported that neurodegenerative disease formation is caused by failure of the autophagy mechanism. This review outlines PKC signaling in autophagy and neurodegenerative disease development and introduces some polyphenols as effectors of PKC isozymes for disease therapy.

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Allium cepa Extract and Quercetin Protect Neuronal Cells from Oxidative Stress via PKC‐ε Inactivation/ERK1/2 Activation

Cited by 31 publications

References 34 publications

Neuroprotective effects of quercetin 4’- O -β- d -diglucoside on human striatal precursor cells in nutrient deprivation condition

Neuroprotective effects of quercetin 4’- O -β- d -diglucoside on human striatal precursor cells in nutrient deprivation condition

Quercetin Has Antimetastatic Effects on Gastric Cancer Cells via the Interruption of uPA/uPAR Function by Modulating NF-κb, PKC-δ, ERK1/2, and AMPKα

Protein Kinase C Isozymes and Autophagy during Neurodegenerative Disease Progression

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