Epigallocatechin gallate prevents oxidative-stress-induced death of mutant Cu/Zn-superoxide dismutase (G93A) motoneuron cells by alteration of cell survival and death signals

Koh, Seong Ho

doi:10.1016/j.tox.2004.05.008

Cited by 72 publications

(50 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Many studies have suggested the protection of catechins, quercetin, and kaempferol, known to be contained in SR, against oxidative stress-induced neuronal damage in cultures and ischemia-induced rat brain damage. [55][56][57][58][59][60] Catechin isolated from SR prevented H 2 O 2 -induced neuronal death in cultures in the present study. It is thus presumed that catechin might be partly responsible for the anti-ischemic effect of SR.…”

Section: Discussionmentioning

confidence: 66%

Neuroprotective Effect of Sanguisorbae Radix against Oxidative Stress-Induced Brain Damage: in Vitro and in Vivo

Nguyen

Cho

Ban

et al. 2008

Biological & Pharmaceutical Bulletin

View full text Add to dashboard Cite

Stroke is the third leading cause of death and an important factor that may affect morbidity and long-term disability. It has been suggested that ischemic stroke may result in the interruption and/or severe reduction of blood flow in cerebral arteries.1) The brain has an absolute dependence on the blood for its immediate supply of oxygen and energy substrates.2)The depletion of energy stores influenced by interruption of the cerebral blood flow can cause several acute metabolic disturbances, such as disruption of ion homeostasis, massive release of excitotoxic amino acids, and free radical formation. The energy failure may lead to membrane depolarization, thus causing reduced activity of ATP-dependent ion pump, Na ϩ /K ϩ -ATPase, which regulates the ionic concentration gradients needed to generate action potentials by neurons.3) The subsequent depolarization of membranes leads to activated glutamate receptors, of which the N-methyl-D-aspartate (NMDA) and a-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA) receptors are clearly implicated in neurotoxicity, and consequently a further increase in Ca 2ϩ levels.2,4,5) Elevated intracellular Ca 2ϩ causes an increase in cellular oxidative stress that contributes to cell damage, and activates various enzymes such as lipases, proteases, and endonucleases that may damage DNA, cell proteins, and lipids, thus leading to cellular death. 4,6) It has been indicated that oxidative stress is considered one of the primary risk factors that exacerbate the damage by cerebral ischemia.7) Several components of reactive oxygen species (ROS) generated after ischemia/reperfusion injury, ), are known to promote DNA damage, peroxidation of lipids, proteins and carbohydrates, blood brain-barrier break-down, and microglial infiltration in the ischemic territory. 4,8,9) Experimental ischemia/reperfusion models have been extensively studied, [15][16][17] and the cumulative evidence suggests involvement of oxygen radicals in the pathogenesis of ischemic lesions. ] i , and inhibiting glutamate release and generation of ROS, and that the neuroprotective effect of SR against focal cerebral ischemic injury is due to its anti-oxidative effects. Thus SR might have therapeutic roles in neurodegenerative diseases such as stroke.

show abstract

Section: Discussionmentioning

confidence: 66%

Neuroprotective Effect of Sanguisorbae Radix against Oxidative Stress-Induced Brain Damage: in Vitro and in Vivo

Nguyen

Cho

Ban

et al. 2008

Biological & Pharmaceutical Bulletin

View full text Add to dashboard Cite

show abstract

“…EGCG suppresses apoptosis in some types of cultured neurons (Choi et al 2001;Koh et al 2004). It is needed to investigate whether the suppressive effect of GT-catechin on brain atrophy is caused, in part, by inhibition of apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Daily consumption of green tea catechin delays memory regression in aged mice

et al. 2006

View full text Add to dashboard Cite

Almost all elderly people show brain atrophy and cognitive dysfunction, even if they are saved from illness, such as cardiac disease, malignancy and diabetes. Prevention or delay of brain senescence would therefore enhance the quality of life for older persons. Because oxidative stress has been implicated in brain senescence, we investigated the effects of green tea catechin (GT-catechin), a potential antioxidant, in senescence-accelerated (SAMP10) mice. The mouse is a model of brain senescence with short life span, cerebral atrophy and cognitive dysfunction. Mice were fed water containing 0.02% GT-catechin from 1- to 15-month-old. The mean dose was about 35 mg/kg/day. We found that daily consumption of GT-catechin prevented memory regression and DNA oxidative damage in these mice. GT-catechin did not prolong the lifetime of SAMP10 mice, but it did delay brain senescence. These findings suggest that continued intake of GT-catechin might promote healthy ageing of the brain in older persons.

show abstract

“…Treatment with epigallocatechin gallate (EGCG) reduced levels of lipid peroxidation and protein oxidation in neurons exposed to advanced glycation end products . EGCG also protected cultured spiral ganglion neurons against hydrogen peroxide (Xie et al, 2004) and cultured motor neurons against oxidative stress induced by a mutation in SOD1 that causes an inherited form of amyotrophic lateral sclerosis (ALS) (Koh et al, 2004). When cultured primary neurons were treated with relatively low concentrations of quercetin prior to exposure to Ab1-42, their accumulation of oxidative damage (4-hydroxynonenal, protein carbonyls, and nitrotyrosine) was reduced (Ansari et al, 2009).…”

Section: A Oxidative Stressmentioning

confidence: 99%

“…The citrus bioflavonoid luteolin reduced Ab generation in "Swedish" mutant APP transgenebearing neuron-like cells and primary neurons, and diosmin (a semishynthetic drug modified from hesperidin) significantly reduced Ab pathology, reduced GSK-3 activity, and disrupted the association of presenilin 1 with APP (Rezai-Zadeh et al, 2009). In addition, EGCG prevented oxidative stress-induced death of motor neurons expressing a mutant form of SOD1 that causes ALS, by activating PI3K/Akt and inhibiting GSK-3b (Koh et al, 2004) Studies relevant to AD have shown that GSK-3b activity promotes Ab production and that GSK-3b directly phosphorylates t, resulting in the formation of neurofibrillary tangle-like filaments (Alonso et al, 2001). Abnormal increases of GSK-3b levels and activity occur in brain cells of patients with AD, and are associated with neuronal death, t pathologies, and a decline in cognitive function (Bhat et al, 2004).…”

Section: Phytochemicals and Adaptive Responsesmentioning

confidence: 99%

Adaptive Cellular Stress Pathways as Therapeutic Targets of Dietary Phytochemicals: Focus on the Nervous System

et al. 2014

View full text Add to dashboard Cite

Epigallocatechin gallate prevents oxidative-stress-induced death of mutant Cu/Zn-superoxide dismutase (G93A) motoneuron cells by alteration of cell survival and death signals

Cited by 72 publications

References 20 publications

Neuroprotective Effect of Sanguisorbae Radix against Oxidative Stress-Induced Brain Damage: in Vitro and in Vivo

Neuroprotective Effect of Sanguisorbae Radix against Oxidative Stress-Induced Brain Damage: in Vitro and in Vivo

Daily consumption of green tea catechin delays memory regression in aged mice

Adaptive Cellular Stress Pathways as Therapeutic Targets of Dietary Phytochemicals: Focus on the Nervous System

Contact Info

Product

Resources

About