Protective Effect of Green Tea Extract on Neuronal Cell Death in Alzheimer Model using beta-amyloid Peptide.
- Author:
Hyun Jung LEE
1
;
Do Yeon LEE
;
Yoo Hun NOH
;
Ji Young YUN
;
Yoon Hee CHUNG
;
Kyung Yong KIM
;
Sung Su KIM
;
Won Bok LEE
Author Information
1. Department of Anatomy, College of Medicine, Chung-Ang University. whitefox@cau.ac.kr
- Publication Type:In Vitro ; Original Article
- Keywords:
beta-amyloid (Abeta);
EGCG;
Neurotoxicity;
Alzheimer's disease
- MeSH:
Alzheimer Disease;
Animals;
Apoptosis;
Caspase 3;
Cell Death*;
Cytochromes c;
Cytosol;
Hippocampus;
In Situ Nick-End Labeling;
Lateral Ventricles;
Learning;
Membrane Potential, Mitochondrial;
Mice;
Mice, Inbred ICR;
Neurons*;
Tea*
- From:Korean Journal of Anatomy
2005;38(6):543-552
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
In the present study, we determined whether green tea extract, EGCG protected against beta-amyloid induced neurotoxicity and learning impairment in vitro and in vivo models. Incubation of SK-N-SH cells with Abeta induced activation of caspase-3, mitochondrial dysfunction such as collapse of mitochondrial membrane potential (MMP) and release of cytosolic cytochrome c. Interestingly, pre-treatment of EGCG reduced significantly activation of caspase-3 and increase of mitochondrial damage such as the breakdown of MMP and release of cytochrome c, eventually attenuated the cell death induced by Abeta. These results show that EGCG inhibited caspase activity and blocked mitochondrial damage. For in vivo experiment, ICR mice received vehicle or vehicle plus EGCG (10 mg/kg) i.p. for 3 days. Before 2 days of treatment, 5 microliter of PBS containing 8 nmol of Abeta1-42 were injected into the lateral ventricle. On the 14th day of treatment, animals were applied to passive avoidance test, and after behavial test, animals were sacrificed. Then, morphological techniques were used to determine the extent of neuronal degeneration in the hippocampus. Abeta, but not PBS, injections into hippocampus led to neuronal loss and evidence of widespread apoptosis. EGCG treated animals had significant reductions in the amount of neuronal degeneration, and TUNEL positive cells compared with Abeta alone treated animals. These data suggest that EGCG at therapeutically relevant concentrations, might protect against neuronal degeneration induced by Abeta.
