Tea vs Neuro-degeneration

Ian Goddard igoddard at erols.mom
Thu Jan 10 01:56:51 EST 2002


Biochemical Pharmacology, 2002 Jan;63(1):21-29:

"Neuroprotection was attributed to the potent antioxidant and 
iron chelating actions of the polyphenolic constituents of tea
extracts, preventing nuclear translocation and activation of 
cell death promoting NF-kappaB. Brain penetrating property 
of polyphenols may make such compounds an important class 
of drugs for treatment of neurodegenerative diseases."


Biochemical Pharmacology, 2002 Jan;63(1):21-29

Attenuation of 6-hydroxydopamine (6-OHDA)-induced nuclear
factor-kappaB (NF-kappaB) activation and cell death by tea 
extracts in neuronal cultures(1).

Levites Y, Youdim MB, Maor G, Mandel S.

Eve Topf and USA National Parkinson Foundation Centers 
of Excellence for Neurodegenerative Diseases Research,
Technion-Faculty of Medicine, Haifa, Israel

Antioxidant and anti-inflammatory therapy approaches have been 
in the focus of attention in the treatment of neurodegenerative
Parkinson's and Alzheimer's diseases where oxidative stress has 
been implicated. Tea extracts have been previously reported to 
possess radical scavenger, iron chelating and anti-inflammatory
properties in a variety of tissues. The purpose of this study
was to investigate potential neuroprotective effects of tea 
extracts and possible signal pathway involved in a neuronal cell 
model of Parkinson's disease. We demonstrated highly potent
antioxidant-radical scavenging activities of green tea (GT) and 
black tea (BT) extracts on brain mitochondrial membrane fraction,
against iron (2.5 &mgr;M)-induced lipid peroxidation. Both extracts
(0.6-3 &mgr;M total polyphenols) were shown to attenuate the
neurotoxic action of 6-hydroxydopamine (6-OHDA)-induced neuronal
death. 6-OHDA (350 and 50 &mgr;M) activated the iron dependent
inflammatory redox sensitive nuclear factor-kappaB (NF-kappaB) in 
rat pheochromocytoma (PC12) and human neuroblastoma (NB) SH-SY5Y
cells, respectively. Immunofluorescence and electromobility shift
assays showed increased nuclear translocation and binding activity 
of NF-kappaB after exposure to 6-OHDA in NB SH-SY5Y cells, with a
concomitant disappearance from the cytoplasm. Introduction of GT
extract (0.6, 3 &mgr;M total polyphenols) before 6-OHDA inhibited 
both NF-kappaB nuclear translocation and binding activity induced 
by this toxin in NB SH-SY5Y cells. Neuroprotection was attributed 
to the potent antioxidant and iron chelating actions of the
polyphenolic constituents of tea extracts, preventing nuclear
translocation and activation of cell death promoting NF-kappaB. 
Brain penetrating property of polyphenols may make such compounds 
an important class of drugs for treatment of neurodegenerative
diseases.

http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11754870&dopt=Abstract


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