아밀로이드 베타 단백질을 이용한 알츠하이머 모델에서 유도되는 신경세포 사멸에 대한 녹차 추출물의 보호 작용에 관한 연구

초록

In the present study, we determined whether green tea extract, EGCG protected against β-amyloid induced neurotoxicity and learning impairment in vitro and in vivo models. Incubation of SK-N-SH cells with Aβ 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 Aβ. 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 µL of PBS containing 8 nmol of Aβ1-42 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. Aβ, 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 Aβ alone treated animals. These data suggest that EGCG at therapeutically relevant concentrations, might protect against neuronal degeneration induced by Aβ.

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