Supplementation with a synthetic polyphenol limits oxidative stress and enhances neuronal cell viability in response to hypoxia–re-oxygenation injury

Duong, T. T. Hong; Antao, Shane; Ellis, Natasha A.; Myers, Simon J.; Witting, Paul K.

doi:10.1016/j.brainres.2008.04.044

Cited by 24 publications

(19 citation statements)

References 44 publications

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“…It has been proposed that flavonoid glycosides like rutin and isoquercitrin induced activation of SOD enzyme in turn catalyzed the detoxification of superoxide radicals to less toxic molecules, and lead to attenuation of oxidative stress. 33 The reduced superoxide radical in cellular system is directly correlated with increased cellular antioxidant capabilities. 34,35 Glutathione peroxidase and glutathione system are powerful antioxidant systems that work together by converting toxic hydroperoxide molecules into water and alcohol.…”

Section: Discussionmentioning

confidence: 99%

Protective effects of quercetin glycosides, rutin, and isoquercetrin against 6-hydroxydopamine (6-OHDA)-induced neurotoxicity in rat pheochromocytoma (PC-12) cells

Magalingam

Radhakrishnan

Haleagrahara

2015

Int J Immunopathol Pharmacol

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There is increasing evidence that free radicals induced oxidative stress is a major causative agent in the pathogenesis of neurodegenerative diseases, particularly Parkinson's disease. Quercetin glycosides, namely rutin and isoquercitrin, are flavonoid polyphenol compounds found ubiquitously in fruits and vegetables and have been known to possess antioxidant effects. This study was designed to compare the neuroprotective effects of quercetin glycosides rutin and isoquercitrin in 6-OHDA-induced rat pheochromocytoma (PC-12) cells. The results showed that both rutin and isoquercitrin significantly increased antioxidant enzymes, catalase, superoxide dismutase, glutathione peroxidase, and glutathione level that were attenuated by 6-OHDA in PC-12 cells. There was no significant difference in the activation of glutathione and glutathione peroxidase enzymes between rutin and isoquercitrin. These two glycosides were equally effective in suppressing lipid peroxidation in 6-OHDA-induced PC-12 cells as both compounds suppressed the malondialdehyde generation and prevented cell damage. In conclusion, quercetin glycosides rutin and isoquercetrin are having a significant neuroprotective effect against 6-OHDA toxicity in PC-12 cells.

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Section: Discussionmentioning

confidence: 99%

Protective effects of quercetin glycosides, rutin, and isoquercetrin against 6-hydroxydopamine (6-OHDA)-induced neurotoxicity in rat pheochromocytoma (PC-12) cells

Magalingam

Radhakrishnan

Haleagrahara

2015

Int J Immunopathol Pharmacol

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“…Glutathione peroxidase (GPx) levels were modulated by red wine polyphenols resulting in combat of oxidative stress [132]. Similarly, phenolic antioxidant 3,3′,5,5′-tetra-t-butyl-biphenyl-4,4′-diol also controlled expression of GPx and HIF-1 α in hypoxia studies [133]. Various polyphenols like butein, phloretin, chrysin, apigenin, and luteolin activated HO-1 (HMOX1), GCLC, and GCLM through expression of ERK/Nrf2 pathway [129, 134].…”

Section: Polyphenols As Neuronal Mitochondria Medicinementioning

confidence: 99%

Polyphenols: Multipotent Therapeutic Agents in Neurodegenerative Diseases

Bhullar

Rupasinghe

2013

Oxidative Medicine and Cellular Longevity

347

194

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Aging leads to numerous transitions in brain physiology including synaptic dysfunction and disturbances in cognition and memory. With a few clinically relevant drugs, a substantial portion of aging population at risk for age-related neurodegenerative disorders require nutritional intervention. Dietary intake of polyphenols is known to attenuate oxidative stress and reduce the risk for related neurodegenerative diseases such as Alzheimer's disease (AD), stroke, multiple sclerosis (MS), Parkinson's disease (PD), and Huntington's disease (HD). Polyphenols exhibit strong potential to address the etiology of neurological disorders as they attenuate their complex physiology by modulating several therapeutic targets at once. Firstly, we review the advances in the therapeutic role of polyphenols in cell and animal models of AD, PD, MS, and HD and activation of drug targets for controlling pathological manifestations. Secondly, we present principle pathways in which polyphenol intake translates into therapeutic outcomes. In particular, signaling pathways like PPAR, Nrf2, STAT, HIF, and MAPK along with modulation of immune response by polyphenols are discussed. Although current polyphenol researches have limited impact on clinical practice, they have strong evidence and testable hypothesis to contribute clinical advances and drug discovery towards age-related neurological disorders.

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“…Bilirubin production was determined with reversed-phase gradient liquid chromatography, with concentrations determined with peak-area comparison with authentic standards (6). In some reactions, fresh preparations of tin [SnPPX(IX)] (Alexis Biochemicals, Plymouth Meeting, PA) dissolved in 0.01N NaOH were added to reaction mixtures at ratios of hemin:metalloporphyrin of 1:1 mol=mol as positive controls, because SnPPX(IX) is a potent inhibitor of HO activity.…”

Section: Assessment Of Myocardial Ho Activitymentioning

confidence: 99%

Endogenous Adenosine Selectively Modulates Oxidant Stressviathe A₁Receptor in Ischemic Hearts

Reichelt

Shanu

Willems

et al. 2009

Antioxidants & Redox Signaling

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We tested the impact of A 1 adenosine receptor (AR) deletion on injury and oxidant damage in mouse hearts subjected to 25-min ischemia=45-min reperfusion (I=R). Wild-type hearts recovered *50% of contractile function and released 8.2 AE 0.7 IU=g of lactate dehydrogenase (LDH). A 1 AR deletion worsened dysfunction and LDH efflux (15.2 AE 2.6 IU=g). Tissue cholesterol and native cholesteryl esters were unchanged, whereas cholesteryl ester-derived lipid hydroperoxides and hydroxides (CE-O(O)H; a marker of lipid oxidation) increased threefold, and a-tocopherylquinone [a-TQ; oxidation product of a-tocopherol (a-TOH)] increased sixfold. Elevations in a-TQ were augmented by two-to threefold by A 1 AR deletion, whereas CE-O(O)H was unaltered. A 1 AR deletion also decreased glutathione redox status ([GSH]=[GSSG + GSH]) and enhanced expression of the antioxidant response element heme oxygenase-1 (HO-1) during I=R: fourfold elevations in HO-1 mRNA and activity were doubled by A 1 AR deletion. Broad-spectrum AR agonism (10 mM 2-chloroadenosine; 2-CAD) countered effects of A 1 AR deletion on oxidant damage, HO-1, and tissue injury, indicating that additional ARs (A 2A , A 2B , and=or A 3 ) can mediate similar actions. These data reveal that local adenosine engages A 1 ARs during I=R to limit oxidant damage and enhance outcome selectively. Control of a-TOH=a-TQ levels may contribute to A 1 AR-dependent cardioprotection.

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Supplementation with a synthetic polyphenol limits oxidative stress and enhances neuronal cell viability in response to hypoxia–re-oxygenation injury

Cited by 24 publications

References 44 publications

Protective effects of quercetin glycosides, rutin, and isoquercetrin against 6-hydroxydopamine (6-OHDA)-induced neurotoxicity in rat pheochromocytoma (PC-12) cells

Protective effects of quercetin glycosides, rutin, and isoquercetrin against 6-hydroxydopamine (6-OHDA)-induced neurotoxicity in rat pheochromocytoma (PC-12) cells

Polyphenols: Multipotent Therapeutic Agents in Neurodegenerative Diseases

Endogenous Adenosine Selectively Modulates Oxidant Stressviathe A₁Receptor in Ischemic Hearts

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Supplementation with a synthetic polyphenol limits oxidative stress and enhances neuronal cell viability in response to hypoxia–re-oxygenation injury

Cited by 24 publications

References 44 publications

Protective effects of quercetin glycosides, rutin, and isoquercetrin against 6-hydroxydopamine (6-OHDA)-induced neurotoxicity in rat pheochromocytoma (PC-12) cells

Protective effects of quercetin glycosides, rutin, and isoquercetrin against 6-hydroxydopamine (6-OHDA)-induced neurotoxicity in rat pheochromocytoma (PC-12) cells

Polyphenols: Multipotent Therapeutic Agents in Neurodegenerative Diseases

Endogenous Adenosine Selectively Modulates Oxidant Stressviathe A1Receptor in Ischemic Hearts

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Endogenous Adenosine Selectively Modulates Oxidant Stressviathe A₁Receptor in Ischemic Hearts