title: Green tea averts age-dependent decline of hippocampal signaling systems related to antioxidant defenses and survival.
abstract: We previously found that prolonged consumption of green tea (GT), a rich source of antioxidant polyphenols, protected proteins and lipids against oxidation and reduced lipofuscin deposition in the rat hippocampal formation as well as improving spatial memory during aging. In this work, we sought to investigate whether GT treatment could interfere with age-related changes in redox status and cellular signaling systems related to oxidative stress and survival in the same brain region. To address this issue, five male Wistar rats were fed with GT from 12 to 19 months of age and results were compared to those obtained from controls age 19 months (C-19 M). A third group of rats was evaluated at 12 months of age to provide baseline data. At completion of the specified time points, the glutathione levels and antioxidant enzyme activities, the activation of the transcription factors cyclic AMP response element-binding (CREB) and nuclear factor-kappaB (NF-kappaB, p50 and p65 subunits), and the levels of brain-derived neurotrophic factor (BDNF) and B-cell lymphoma-2 (Bcl-2) were measured in hippocampal formations. GT-treated rats presented higher reduced and lower oxidized glutathione levels and displayed favorable alterations in antioxidant enzyme activities compared to C-19 M animals. In addition, GT increased CREB activation and the levels of BDNF and Bcl-2, but had no effect on activation of NF-kappaB subunits, relative to age-matched controls. We conclude that long-term GT ingestion improves antioxidant systems and activates CREB in the aging rat hippocampal formation, leading to neuroprotection mediated by downstream upregulation of BDNF and Bcl-2.
authors.affiliation: Department of Anatomy, Faculty of Medicine, University of Porto, 4200-319 Porto, Portugal.
authors.forename: Marco
authors.initials: M
authors.lastname: Assunção
authors.forename: Maria J
authors.initials: MJ
authors.lastname: Santos-Marques
authors.forename: Félix
authors.initials: F
authors.lastname: Carvalho
authors.forename: José P
authors.initials: JP
authors.lastname: Andrade
mesh_terms: D000375:Aging / Q000187:drug effects* / Q000378:metabolism; D000818:Animals; D000975:Antioxidants / Q000008:administration & dosage / Q000378:metabolism / Q000494:pharmacology*; D019208:Brain-Derived Neurotrophic Factor / Q000378:metabolism; D028241:Camellia sinensis / Q000737:chemistry*; D002470:Cell Survival / Q000187:drug effects; D017362:Cyclic AMP Response Element-Binding Protein / Q000378:metabolism; D006624:Hippocampus / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000187:drug effects; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D015398:Signal Transduction / Q000187:drug effects*; D013662:Tea / Q000378:metabolism*
chemical_list: D000975:Antioxidants; D019208:Brain-Derived Neurotrophic Factor; D017362:Cyclic AMP Response Element-Binding Protein; D019253:Proto-Oncogene Proteins c-bcl-2; D013662:Tea