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Inhibitory effect of green tea extract on beta-amyloid-induced PC12 cell death by inhibition of the activation of NF-kappaB and ERK/p38 MAP kinase pathway through antioxidant mechanisms.
Brain Res Mol Brain Res. 2005 Oct 31; 140(1-2):45-54.BR

Abstract

Beta-amyloid peptide (Abeta) is considered responsible for the pathogenesis of Alzheimer's disease (AD). Several lines of evidence support that Abeta-induced cytotoxicity is mediated through the generation of reactive oxygen species (ROS). Thus, agents that scavenge ROS level may usefully impede the development or progress of AD. Green tea extract has been known to have such antioxidant properties. Our previous studies demonstrate that green tea extract protected ischemia/reperfusion-induced brain cell death by scavenging oxidative damages of macromolecules. In this study, we investigated the effects of green tea extract on Abeta-induced oxidative cell death in cultured rat pheochromocytoma (PC12) cells. PC12 cells treated with Abeta25-35 (10-50 microM) showed intracellular ROS elevation, the formation of 8-oxodG (an oxidized form of DNA), and underwent apoptotic cell death in a dose-dependent manner. Abeta(25-35) treatment upregulated pro-apoptotic p53 at the gene level, and Bax and caspase-3 at the protein level, but downregulated anti-apoptotic Bcl-2 protein. Interestingly, co-treated green tea extract (10-50 microg/ml) dose-dependently attenuated Abeta(25-35) (50 microM)-induced cell death, intracellular ROS levels, and 8-oxodG formation, in addition to p53, Bax, and caspase-3 expression, but upregulated Bcl-2. Furthermore, green tea extract prevented the Abeta(25-35)-induced activations of the NF-kappaB and ERK and p38 MAP kinase pathways. Our study suggests that green tea extract may usefully prevent or retard the development and progression of AD.

Authors+Show Affiliations

College of Pharmacy, Chungbuk National University, 48, Gaesin-dong, Heungduk-gu, Cheongju, Chungbuk 361-763, South Korea.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

16153742

Citation

Lee, Sun Young, et al. "Inhibitory Effect of Green Tea Extract On Beta-amyloid-induced PC12 Cell Death By Inhibition of the Activation of NF-kappaB and ERK/p38 MAP Kinase Pathway Through Antioxidant Mechanisms." Brain Research. Molecular Brain Research, vol. 140, no. 1-2, 2005, pp. 45-54.
Lee SY, Lee JW, Lee H, et al. Inhibitory effect of green tea extract on beta-amyloid-induced PC12 cell death by inhibition of the activation of NF-kappaB and ERK/p38 MAP kinase pathway through antioxidant mechanisms. Brain Res Mol Brain Res. 2005;140(1-2):45-54.
Lee, S. Y., Lee, J. W., Lee, H., Yoo, H. S., Yun, Y. P., Oh, K. W., Ha, T. Y., & Hong, J. T. (2005). Inhibitory effect of green tea extract on beta-amyloid-induced PC12 cell death by inhibition of the activation of NF-kappaB and ERK/p38 MAP kinase pathway through antioxidant mechanisms. Brain Research. Molecular Brain Research, 140(1-2), 45-54.
Lee SY, et al. Inhibitory Effect of Green Tea Extract On Beta-amyloid-induced PC12 Cell Death By Inhibition of the Activation of NF-kappaB and ERK/p38 MAP Kinase Pathway Through Antioxidant Mechanisms. Brain Res Mol Brain Res. 2005 Oct 31;140(1-2):45-54. PubMed PMID: 16153742.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Inhibitory effect of green tea extract on beta-amyloid-induced PC12 cell death by inhibition of the activation of NF-kappaB and ERK/p38 MAP kinase pathway through antioxidant mechanisms. AU - Lee,Sun Young, AU - Lee,Jae Woong, AU - Lee,Heesoon, AU - Yoo,Han Soo, AU - Yun,Yeo Pyo, AU - Oh,Ki Wan, AU - Ha,Tae Youl, AU - Hong,Jin Tae, Y1 - 2005/09/08/ PY - 2004/09/20/received PY - 2005/06/11/revised PY - 2005/07/09/accepted PY - 2005/9/13/pubmed PY - 2006/2/4/medline PY - 2005/9/13/entrez SP - 45 EP - 54 JF - Brain research. Molecular brain research JO - Brain Res Mol Brain Res VL - 140 IS - 1-2 N2 - Beta-amyloid peptide (Abeta) is considered responsible for the pathogenesis of Alzheimer's disease (AD). Several lines of evidence support that Abeta-induced cytotoxicity is mediated through the generation of reactive oxygen species (ROS). Thus, agents that scavenge ROS level may usefully impede the development or progress of AD. Green tea extract has been known to have such antioxidant properties. Our previous studies demonstrate that green tea extract protected ischemia/reperfusion-induced brain cell death by scavenging oxidative damages of macromolecules. In this study, we investigated the effects of green tea extract on Abeta-induced oxidative cell death in cultured rat pheochromocytoma (PC12) cells. PC12 cells treated with Abeta25-35 (10-50 microM) showed intracellular ROS elevation, the formation of 8-oxodG (an oxidized form of DNA), and underwent apoptotic cell death in a dose-dependent manner. Abeta(25-35) treatment upregulated pro-apoptotic p53 at the gene level, and Bax and caspase-3 at the protein level, but downregulated anti-apoptotic Bcl-2 protein. Interestingly, co-treated green tea extract (10-50 microg/ml) dose-dependently attenuated Abeta(25-35) (50 microM)-induced cell death, intracellular ROS levels, and 8-oxodG formation, in addition to p53, Bax, and caspase-3 expression, but upregulated Bcl-2. Furthermore, green tea extract prevented the Abeta(25-35)-induced activations of the NF-kappaB and ERK and p38 MAP kinase pathways. Our study suggests that green tea extract may usefully prevent or retard the development and progression of AD. SN - 0169-328X UR - https://www.unboundmedicine.com/medline/citation/16153742/Inhibitory_effect_of_green_tea_extract_on_beta_amyloid_induced_PC12_cell_death_by_inhibition_of_the_activation_of_NF_kappaB_and_ERK/p38_MAP_kinase_pathway_through_antioxidant_mechanisms_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0169-328X(05)00299-8 DB - PRIME DP - Unbound Medicine ER -