3′,4′-Didemethylnobiletin induces phase II detoxification gene expression and modulates PI3K/Akt signaling in PC12 cells

Su, Jeng Dian; Yen, Jui-Hung; Li, Shiming; Weng, Ching Yi; Lin, Ming Hwai; Ho, Chi‐Tang; Wu, Ming-Jiuan

doi:10.1016/j.freeradbiomed.2011.10.002

Cited by 56 publications

(27 citation statements)

References 84 publications

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“…This value was calculated to be ≈ 900 μM in contrast to the found by Zhang et al [37], who reported that ARPE-19 cells needed 24 h to develop half cytotoxicity effect at 300 μM nominal concentration but the cells were grown in serum starvation in DMEM/F-12 Su et al [52] reported similar behavior when neuronal cells were cultured in serum-free medium for 48 h they experienced about 40 % cell death. This cell population displayed decrease in S phase and an emergence of sub-G 0 /G 1 phase compared with those cultured in normal serum.…”

Section: Discussionmentioning

confidence: 59%

Retino-protective effect of Bucida buceras against oxidative stress induced by H2O2 in human retinal pigment epithelial cells line

Assanga¹,

Lewis-Luján²,

Fernández-Angulo

et al. 2015

BMC Complement Altern Med

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BackgroundReactive Oxygen Species (ROS) impair the physiological functions of Retinal Pigment Epithelial (RPE) cells, which are known as one major cause of age-related macular degeneration and retinopathy diseases. The purpose of this study is to explore the cytoprotective effects of the antioxidant Bucida buceras extract in co-treatment with hydrogen peroxide (H2O2) delivery as a single addition or with continuous generation using glucose oxidase (GOx) in ARPE-19 cell cultures. The mechanism of Bucida buceras extract is believed to be associated with their antioxidant capacity to protect cells against oxidative stress.MethodsA comparative oxidative stress H2O2-induced was performed by addition and enzymatic generation using glucose oxidase on human retinal pigment epithelial cells line. H2O2-induced injury was measured by toxic effects (cell death and apoptotic pathway) and intracellular redox status: glutathione (GSH), antioxidant enzymes (catalase and glutathione peroxidase) and reducing power (FRAP). The retino-protective effect of co-treatment with Bucida buceras extract on H2O2-induced human RPE cell injury was investigated by cell death (MTT assay) and oxidative stress biomarkers (H2O2, GSH, CAT, GPx and FRAP).ResultsBucida buceras L. extract is believed to be associated with the ability to prevent cellular oxidative stress. When added as a pulse, H2O2 is rapidly depleted and the cytotoxicity analyses show that cells can tolerate short exposure to high peroxide doses delivered as a pulse but are susceptible to lower chronic doses. Co-treatment with Bucida buceras was able to protect the cells against H2O2-induced injury. In addition to preventing cell death treatment with antioxidant plant could also reverse the significant decrease in GSH level, catalase activity and reducing power caused by H2O2.ConclusionThese findings suggest that Bucida buceras could protect RPE against ocular pathogenesis associated with oxidative stress induced by H2O2-delivered by addition and enzymatic generation.

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Section: Discussionmentioning

confidence: 59%

Retino-protective effect of Bucida buceras against oxidative stress induced by H2O2 in human retinal pigment epithelial cells line

Assanga¹,

Lewis-Luján²,

Fernández-Angulo

et al. 2015

BMC Complement Altern Med

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“…13,14) It has been reported that several plant-derived polyphenolic compounds can exert neuroprotective action through the regulation of HO-1 expression. 44) Keeping this in consideration, the influence of this flavonoid on HO-1 expression was investigated in the H 2 O 2 -treated cells in order to further understand the molecular mechanism(s) underlying its neuroprotective activity.…”

Section: Discussionmentioning

confidence: 99%

“…[10][11][12] Heme oxygenase (HO)-1, also known as heat shock protein 32, is one of the Phase II detoxification enzymes which in various cell types acts as a key molecule in the cellular maintenance of adaptive survival response to stimuli such as oxidative stress. 13,14) HO-1 catalyzes the oxidative cleavage of heme in the presence of reduced nicotinamide adenine dinucleotide phosphate (NADPH) and oxygen to produce biliverdin, Fe 2+ and CO. Biliverdin is subsequently converted to bilirubin under the action of cytosolic enzyme biliverdin reductase.…”

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confidence: 99%

Protection of Cultured Cortical Neurons by Luteolin against Oxidative Damage through Inhibition of Apoptosis and Induction of Heme Oxygenase-1

Kim

Chin

Cho

2017

Biological & Pharmaceutical Bulletin

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“…Given that oxidative stress is related to the development of learning and memory impairment in SAMP8 mice,42) nobiletin potentially improves cognitive impairment in SAMP8 mice, at least in part, by reducing oxidative stress through modulation of endogenous antioxidant defense systems in the brain. Accordingly, recent in vitro studies also showed the antioxidant properties of nobiletin 53,54,55,56)…”

Section: Main Subjectsmentioning

confidence: 94%

Anti-dementia Activity of Nobiletin, a Citrus Flavonoid: A Review of Animal Studies

Nakajima

Ohizumi

Yamada

2014

Clin Psychopharmacol Neurosci

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Alzheimer's disease (AD), the most common form of dementia among the elderly, is characterized by the progressive decline of cognitive function and has a detrimental impact worldwide. Despite intensive laboratory and clinical research over the last three decades, pharmacological options for the prevention and effective long-term treatment of AD are not currently available. Consequently, successful therapeutic and preventive treatments for AD are needed. When researching materials from natural resources having anti-dementia drug activity, we identified nobiletin, a polymethoxylated flavone from the peel of Citrus depressa. Nobiletin exhibited memory-improving effects in various animal models of dementia and exerted a wide range of beneficial effects against pathological features of AD including amyloid-β (Aβ) pathology, tau hyperphosphorylation, oxidative stress, cholinergic neurodegeneration and dysfunction of synaptic plasticity-related signaling, suggesting this natural compound could become a novel drug for the treatment and prevention of AD.

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3′,4′-Didemethylnobiletin induces phase II detoxification gene expression and modulates PI3K/Akt signaling in PC12 cells

Cited by 56 publications

References 84 publications

Retino-protective effect of Bucida buceras against oxidative stress induced by H2O2 in human retinal pigment epithelial cells line

Retino-protective effect of Bucida buceras against oxidative stress induced by H2O2 in human retinal pigment epithelial cells line

Protection of Cultured Cortical Neurons by Luteolin against Oxidative Damage through Inhibition of Apoptosis and Induction of Heme Oxygenase-1

Anti-dementia Activity of Nobiletin, a Citrus Flavonoid: A Review of Animal Studies

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