Redox Processes in Neurodegenerative Disease Involving Reactive Oxygen Species

Kovacic, Peter; Somanathan, Ratnasamy

doi:10.2174/157015912804499429

Cited by 40 publications

(18 citation statements)

References 92 publications

(96 reference statements)

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“…However, advanced aging, genetic mutations or long-term environmental exposure could accelerate the production of ROS, which activates pro-apoptotic signalling or inhibits pro-survival signal and finally leads to cell death [48][49][50][51]. However, advanced aging, genetic mutations or long-term environmental exposure could accelerate the production of ROS, which activates pro-apoptotic signalling or inhibits pro-survival signal and finally leads to cell death [48][49][50][51].…”

Section: Dj-1 and Rack1 Were Correlatively Decreased In The Cellular mentioning

confidence: 99%

DJ-1 interacts with RACK1 and protects neurons from oxidative-stress-induced apoptosis

Zhang

et al. 2014

Biochemical Journal

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PD (Parkinson's disease) is a complex disorder that is associated with neuronal loss or dysfunction caused by genetic risks, environmental factors and advanced aging. It has been reported that DJ-1 mutations rendered neurons sensitive to oxidative damage, which led to the onset of familiar PD. However, the molecular mechanism is still unclear. In the present study we show that DJ-1 interacts with RACK1 (receptor of activated C kinase 1) and increases its dimerization and protein stability. The DJ-1 transgene protects cortical neurons from H2O2-induced apoptosis, and this protective effect is abrogated by knocking down RACK1. Similarly, deletion of DJ-1 in cortical neurons increases the sensitivity to H2O2, and the damage can be significantly rescued by DJ-1 or DJ-1/RACK1 co-transfection, but not by RACK1 alone. We observed further that the interaction of DJ-1 and RACK1 is disrupted by H2O2 or MPP+ (1-methyl-4-phenylpyridinium) treatment, and the protein levels of DJ-1 and RACK1 decreased in neurodegenerative disease models. Taken together, the DJ-1-RACK1 complex protects neurons from oxidative stress-induced apoptosis, with the implication that DJ-1 and RACK1 might be novel targets in the treatment of neurodegenerative diseases.

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Section: Dj-1 and Rack1 Were Correlatively Decreased In The Cellular mentioning

confidence: 99%

DJ-1 interacts with RACK1 and protects neurons from oxidative-stress-induced apoptosis

Zhang

et al. 2014

Biochemical Journal

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“…The pathogenesis of neurological disorders is still not clearly identified, and oxidative stress in neuronal cell has been proposed to play roles in disease processes [1–2]. The oxidative stress status of cell and tissue could be altered by exposure to oxidants.…”

Section: Introductionmentioning

confidence: 99%

Asarone from Acori Tatarinowii Rhizome prevents oxidative stress-induced cell injury in cultured astrocytes: A signaling triggered by Akt activation

et al. 2017

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Acori Tatarinowii Rhizome (ATR; the dried rhizome of Acori tatarinowii Schott) is a well-known herb being used for mental disorder in China and Asia. Volatile oil is considered as the active ingredient of ATR, and asarones account for more than 90% of total volatile oil. Here, the protective effects of ATR oil and asarones, both α-asarone and β-asarone, were probed in cultured rat astrocytes. The cyto-protective effect of ATR oil and asarones against tBHP-induced astrocyte injury was revealed, and additionally ATR oil and asarones reduced the tBHP-induced intracellular reactive oxygen species (ROS) accumulation. In parallel, the activity of anti-oxidant response element (ARE) promoter construct (pARE-Luc), being transfected in cultured astrocytes, was markedly induced by application of ATR oil and asarones. The mRNAs encoding anti-oxidant enzymes, e.g. glutathione S-transferase (GST), glutamate-cysteine ligase modulatory subunit (GCLM), glutamate-cysteine ligase catalytic subunit (GCLC) and NAD(P)H quinone oxidoreductase (NQO1) were induced by ATR oil and asarones in a dose-dependent manner. The ATR oil/asarone-induced gene expression could be mediated by Akt phosphorylation; because the applied LY294002, a phosphoinositide 3-kinase inhibitor, fully abolished the induction. These results demonstrated that α-asarone and β-asarone could account, at least partly, the function of ATR being a Chinese medicinal herb.

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“…). Studies have also shown that QA may form complexes with iron and electron transfer from these complexes to oxygen result in increased ROS production (Guillemin ; Kovacic and Ratnasamy ). QA–Fe 2+ complexes may also initiate the Fenton reaction in which highly reactive hydroxyl radicals are formed (Guillemin ).…”

Section: Resultsmentioning

confidence: 99%

Chromatographic Fingerprint Analysis, Acetylcholinesterase Inhibitory Properties and Antioxidant Activities of Redflower Ragleaf (C rassocephalum Crepidioides) Extract

Adefegha

Oboh

Molehin

et al. 2015

Journal of Food Biochemistry

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Consumption of vegetables has been suggested to be a practical strategy in the management of several degenerative diseases. The present study characterized the phenolic constituents, assessed the acetylcholinesterase inhibitory effect and evaluated the antioxidant properties of hydrophilic extracts of redflower ragleaf (Crassocephalum crepidioides [Benth.] S. Moore [Asteraceae]) used as food and traditional medicine in Africa. The vegetable extract was found to be rich in phenolic acids (chlorogenic acid and caffeic acid) and flavonoids (quercetin and rutin). Furthermore, the extract (IC50 = 139.75 μg/mL) inhibited acetylcholinesterase activity in a dose‐dependent manner and had high antioxidant properties as typified by the radical scavenging abilities, reducing property, Fe2+ chelating ability and inhibition of lipid peroxidation in brain tissue (in vitro). These results reveal that the vegetable extract is a rich source of phenolic compounds with antioxidant and acetylcholinesterase inhibitory potential. Practical Applications Redflower ragleaf (Crassocephalum crepidioides) may be a good source of potential phenolic phytochemicals that act as natural antioxidants and acetylcholinesterase inhibitors, and may be beneficial for treatment of Alzheimer's disease.

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Redox Processes in Neurodegenerative Disease Involving Reactive Oxygen Species

Cited by 40 publications

References 92 publications

DJ-1 interacts with RACK1 and protects neurons from oxidative-stress-induced apoptosis

DJ-1 interacts with RACK1 and protects neurons from oxidative-stress-induced apoptosis

Asarone from Acori Tatarinowii Rhizome prevents oxidative stress-induced cell injury in cultured astrocytes: A signaling triggered by Akt activation

Chromatographic Fingerprint Analysis, Acetylcholinesterase Inhibitory Properties and Antioxidant Activities of Redflower Ragleaf (C rassocephalum Crepidioides) Extract

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