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Multifunctional activities of green tea catechins in neuroprotection. Modulation of cell survival genes, iron-dependent oxidative stress and PKC signaling pathway.
Neurosignals. 2005; 14(1-2):46-60.N

Abstract

Many lines of evidence suggest that oxidative stress resulting in reactive oxygen species (ROS) generation and inflammation play a pivotal role in the age-associated cognitive decline and neuronal loss in neurodegenerative diseases including Alzheimer's (AD), Parkinson's (PD) and Huntington's diseases. One cardinal chemical pathology observed in these disorders is the accumulation of iron at sites where the neurons die. The buildup of an iron gradient in conjunction with ROS (superoxide, hydroxyl radical and nitric oxide) are thought to constitute a major trigger in neuronal toxicity and demise in all these diseases. Thus, promising future treatment of neurodegenerative diseases and aging depends on availability of effective brain permeable, iron-chelatable/radical scavenger neuroprotective drugs that would prevent the progression of neurodegeneration. Tea flavonoids (catechins) have been reported to possess potent iron-chelating, radical-scavenging and anti-inflammatory activities and to protect neuronal death in a wide array of cellular and animal models of neurological diseases. Recent studies have indicated that in addition to the known antioxidant activity of catechins, other mechanisms such as modulation of signal transduction pathways, cell survival/death genes and mitochondrial function, contribute significantly to the induction of cell viability. This review will focus on the multifunctional properties of green tea and its major component (-)-epigallocatechin-3-gallate (EGCG) and their ability to induce neuroprotection and neurorescue in vitro and in vivo. In particular, their transitional metal (iron and copper) chelating property and inhibition of oxidative stress.

Authors+Show Affiliations

Eve Topf and USA National Parkinson Foundation Centers of Excellence for Neurodegenerative Diseases Research, Technion-Faculty of Medicine, Haifa, Israel.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

15956814

Citation

Mandel, Silvia A., et al. "Multifunctional Activities of Green Tea Catechins in Neuroprotection. Modulation of Cell Survival Genes, Iron-dependent Oxidative Stress and PKC Signaling Pathway." Neuro-Signals, vol. 14, no. 1-2, 2005, pp. 46-60.
Mandel SA, Avramovich-Tirosh Y, Reznichenko L, et al. Multifunctional activities of green tea catechins in neuroprotection. Modulation of cell survival genes, iron-dependent oxidative stress and PKC signaling pathway. Neurosignals. 2005;14(1-2):46-60.
Mandel, S. A., Avramovich-Tirosh, Y., Reznichenko, L., Zheng, H., Weinreb, O., Amit, T., & Youdim, M. B. (2005). Multifunctional activities of green tea catechins in neuroprotection. Modulation of cell survival genes, iron-dependent oxidative stress and PKC signaling pathway. Neuro-Signals, 14(1-2), 46-60.
Mandel SA, et al. Multifunctional Activities of Green Tea Catechins in Neuroprotection. Modulation of Cell Survival Genes, Iron-dependent Oxidative Stress and PKC Signaling Pathway. Neurosignals. 2005;14(1-2):46-60. PubMed PMID: 15956814.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Multifunctional activities of green tea catechins in neuroprotection. Modulation of cell survival genes, iron-dependent oxidative stress and PKC signaling pathway. AU - Mandel,Silvia A, AU - Avramovich-Tirosh,Yael, AU - Reznichenko,Lydia, AU - Zheng,Hailin, AU - Weinreb,Orly, AU - Amit,Tamar, AU - Youdim,Moussa B H, PY - 2005/01/28/received PY - 2005/03/01/accepted PY - 2005/6/16/pubmed PY - 2005/8/19/medline PY - 2005/6/16/entrez SP - 46 EP - 60 JF - Neuro-Signals JO - Neurosignals VL - 14 IS - 1-2 N2 - Many lines of evidence suggest that oxidative stress resulting in reactive oxygen species (ROS) generation and inflammation play a pivotal role in the age-associated cognitive decline and neuronal loss in neurodegenerative diseases including Alzheimer's (AD), Parkinson's (PD) and Huntington's diseases. One cardinal chemical pathology observed in these disorders is the accumulation of iron at sites where the neurons die. The buildup of an iron gradient in conjunction with ROS (superoxide, hydroxyl radical and nitric oxide) are thought to constitute a major trigger in neuronal toxicity and demise in all these diseases. Thus, promising future treatment of neurodegenerative diseases and aging depends on availability of effective brain permeable, iron-chelatable/radical scavenger neuroprotective drugs that would prevent the progression of neurodegeneration. Tea flavonoids (catechins) have been reported to possess potent iron-chelating, radical-scavenging and anti-inflammatory activities and to protect neuronal death in a wide array of cellular and animal models of neurological diseases. Recent studies have indicated that in addition to the known antioxidant activity of catechins, other mechanisms such as modulation of signal transduction pathways, cell survival/death genes and mitochondrial function, contribute significantly to the induction of cell viability. This review will focus on the multifunctional properties of green tea and its major component (-)-epigallocatechin-3-gallate (EGCG) and their ability to induce neuroprotection and neurorescue in vitro and in vivo. In particular, their transitional metal (iron and copper) chelating property and inhibition of oxidative stress. SN - 1424-862X UR - https://www.unboundmedicine.com/medline/citation/15956814/Multifunctional_activities_of_green_tea_catechins_in_neuroprotection__Modulation_of_cell_survival_genes_iron_dependent_oxidative_stress_and_PKC_signaling_pathway_ L2 - https://www.karger.com?DOI=10.1159/000085385 DB - PRIME DP - Unbound Medicine ER -