Epigallocatechin 3-gallate attenuates neuronal damage induced by 3-hydroxykynurenine

Jeong, Ji Hoon; Kim, Hyung Jun; Lee, Tae Jin; Kim, Mi Kyung; Park, Eon Sub; Choi, Byung Sun

doi:10.1016/j.tox.2003.08.007

Cited by 53 publications

(42 citation statements)

References 28 publications

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“…We couldn't confirm actions of EGCG against 3-HK induced neurocytotoxicity in SH-SY5Y cell line reported earlier by Jeong et al [33]. At the same reported concentration of 10 μM no cytoprotective effects were observed [33].…”

Section: Discussioncontrasting

confidence: 71%

Additive Protective Effects of Luteolin and Pyruvate against 6-Hydroxydopamine and 3-Hydroxykynurenine Induced Neurotoxicity in SH-SY5Y Cells

Wszelaki¹,

Melzig²

2013

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Oxidative stress has been implicated as one of the causes in cell death in many neurodegenerative disorders. Due to antioxidative properties in vitro, the use of flavonoids and other polyphenolic compounds synthesised by plants are considered to be a promising strategy to prevent Alzheimer's disease and Parkinsons's disease. In the present study, we tested protective effects of some polyphenols and sodium pyruvate on 6-hydroxydopamine (6-OHDA), salsolinol and 3-hydroxykynurenine (3-HK) induced neurotoxicity in human neuroblastoma SH-SY5Y cells. We found that luteolin prevented from 6-OHDA and 3-HK induced cell viability reduction and that one of the mechanisms involved in the neuroprotective process was the ability to increase the level of cellular ATP. However, luteolin was ineffective against salsolinol-induced toxicity. Neither pre-treatment with flavonoids nor simultaneous addition had any protective effects on 6-OHDA, salsolinol or 3-HK induced neurotoxicity. Interestingly, both pre-treatment and co-treatment with pyruvate provided protection against 6-OHDA, salsolinol or 3-HK induced toxicity. Moreover, luteolin and sodium pyruvate, administered together, acted additively, so to achieve the same effect, lower concentrations were needed. The ability of luteolin and sodium pyruvate to reduce toxicity of 6-OHDA and 3-HK in SH-SY5Y cells may be related to two different neuroprotective mechanisms and the capability to penetrate into the cell.

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Section: Discussioncontrasting

confidence: 71%

Additive Protective Effects of Luteolin and Pyruvate against 6-Hydroxydopamine and 3-Hydroxykynurenine Induced Neurotoxicity in SH-SY5Y Cells

Wszelaki¹,

Melzig²

2013

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“…Green tea, one of the world's most widely consumed beverages, contains a number of these biologically active polyphenolic compounds, suggesting that the active components of green tea may be beneficial and neuroprotective in conditions of increased oxidative load. Recent studies have demonstrated the neuroprotective activity of GTP in animal models of neurodegenerative conditions such as Parkinson's and Alzheimer's disease and their ability to markedly reduce hypoxic-ischemic tissue loss in models of ischemic stroke through inhibition of caspase-3 activation and proteolytic cleavage of its substrates (31)(32)(33)(34). Although the potential mechanisms whereby GTP may prevent neurological deficits remain to be fully elucidated, recent evidence suggests that GTP may operate as potent free oxygen radical scavengers and protect the brain and other Relative prostaglandin E 2 (PGE 2 ) production in the hippocampal CA1 region of rats exposed to room air (RA) or intermittent hypoxia (IH) and treated with green tea polyphenols (GTP) or vehicle (n 5 3 per group; *P , 0.05, # P , 0.05 vs. RA).…”

Section: Discussionmentioning

confidence: 99%

Green Tea Catechin Polyphenols Attenuate Behavioral and Oxidative Responses to Intermittent Hypoxia

Burckhardt

Gozal²,

Dayyat³

et al. 2008

Am J Respir Crit Care Med

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Rationale: The intermittent hypoxia (IH) that characterizes sleepdisordered breathing impairs spatial learning and increases NADPH oxidase activity and oxidative stress in rodents. We hypothesized that green tea catechin polyphenols (GTPs) may attenuate IHinduced neurobehavioral deficits by reducing IH-induced NADPH oxidase expression, lipid peroxidation, and inflammation. Objectives: To assess the effects of GTP administered in drinking water on the cognitive, inflammatory, and oxidative responses to long-term (.14 d) IH during sleep in male Sprague-Dawley rats. Methods: Cognitive assessments were conducted in the Morris water maze. We measured levels and expression of malondialdehyde (MDA), prostaglandin E 2 , p47 phox subunit of NADPH oxidase, receptor for advanced glycation end products (RAGE), and glial fibrillary acidic protein expression in rodent brain tissue. Measurements and Main Results: GTP treatment prevented IH-induced decreases in spatial bias for the hidden platform during the Morris water maze probe trails as well as IH-induced increases in p47phox expression within the hippocampal CA1 region. In untreated animals, IH exposure was associated with doubling of cortical MDA levels in comparison to room air control animals, and GTP-treated animals exposed to IH showed a 40% reduction in MDA levels. Increases in brain RAGE and glial fibrillary acidic protein expression were observed in IH-exposed animals, and these increases were attenuated in animals treated with GTP. Conclusions: Oral GTP attenuates IH-induced spatial learning deficits and mitigates IH-induced oxidative stress through multiple beneficial effects on oxidant pathways. Because oxidative processes underlie neurocognitive deficits associated with IH, the potential therapeutic role of GTP in sleep-disordered breathing deserves further exploration.

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“…23 Neurotoxicity of KYN and its metabolites has been demonstrated in animal studies 19,20,24 and studies using human cell cultures. 25,26 KYN is able to pass the BBB 27 and human microglia have been shown capable of metabolizing this substance into its toxic metabolites. 28 In addition, peripherally immune-induced IDO activation has been shown to increase QUIN in both plasma and CSF with a highly significant correlation between the two measurements.…”

mentioning

confidence: 99%

IDO and interferon-α-induced depressive symptoms: a shift in hypothesis from tryptophan depletion to neurotoxicity

et al. 2004

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Studies show that administration of interferon (IFN)-a causes a significant increase in depressive symptoms. The enzyme indoleamine 2,3-dioxygenase (IDO), which converts tryptophan (TRP) into kynurenine (KYN) and which is stimulated by proinflammatory cytokines, may be implicated in the development of IFN-a-induced depressive symptoms, first by decreasing the TRP availability to the brain and second by the induction of the KYN pathway resulting in the production of neurotoxic metabolites. Sixteen patients with chronic hepatitis C, free of psychiatric disorders and eligible for IFN-a treatment, were recruited. Depressive symptoms were measured using the Montgomery Asberg Depression Rating Scale (MADRS). Measurements of TRP, amino acids competing with TRP for entrance through the blood-brain barrier, KYN and kynurenic acid (KA), a neuroprotective metabolite, were performed using high-performance liquid chromatography. All assessments were carried out at baseline and 1, 2, 4, 8, 12 and 24 weeks after treatment was initiated. The MADRS score significantly increased during IFN-a treatment as did the KYN/TRP ratio, reflecting IDO activity, and the KYN/KA ratio, reflecting the neurotoxic challenge. The TRP/CAA (competing amino acids) ratio, reflecting TRP availability to the brain, did not significantly change during treatment. Total MADRS score was significantly associated over time with the KYN/KA ratio, but not with the TRP/CAA ratio. Although no support was found that IDO decreases TRP availability to the brain, this study does support a role for IDO activity in the pathophysiology of IFN-a-induced depressive symptoms, through its induction of neurotoxic KYN metabolites. Molecular Psychiatry (2005) 10, 538-544.

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Epigallocatechin 3-gallate attenuates neuronal damage induced by 3-hydroxykynurenine

Cited by 53 publications

References 28 publications

Additive Protective Effects of Luteolin and Pyruvate against 6-Hydroxydopamine and 3-Hydroxykynurenine Induced Neurotoxicity in SH-SY5Y Cells

Additive Protective Effects of Luteolin and Pyruvate against 6-Hydroxydopamine and 3-Hydroxykynurenine Induced Neurotoxicity in SH-SY5Y Cells

Green Tea Catechin Polyphenols Attenuate Behavioral and Oxidative Responses to Intermittent Hypoxia

IDO and interferon-α-induced depressive symptoms: a shift in hypothesis from tryptophan depletion to neurotoxicity

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