Use este identificador para citar ou linkar para este item: https://repositorio.inpa.gov.br/handle/1/15675
Título: Guarana (Paullinia cupana) Extract Protects Caenorhabditis elegans Models for Alzheimer Disease and Huntington Disease through Activation of Antioxidant and Protein Degradation Pathways
Autor: Boasquívis, Patrícia Ferreira
Silva, Giovanna Melo Martins
Paiva, Franciny Aparecida
Cavalcanti, Rodrigo Marinho
Nunez, C. V.
Paula Oliveira, Riva de
Palavras-chave: Amyloid Beta Protein
Caffeine
Catechin
Epicatechin
Extracellular Superoxide Dismutase
Glutathione Transferase 4
Guarana Extract
Methylxanthine
Polyglutamine
Proteasome
Protein
Theobromine
Transcription Factor
Transcription Factor Daf 16
Transcription Factors Skn 1
Unclassified Drug
Antioxidant
Plant Extract
Alzheimer Disease
Animals Experiment
Animals Model
Antioxidant Activity
Autophagosome
Bacterial Growth
Caenorhabditis Elegans
Controlled Study
Dpph Radical Scavenging Assay
Heat Tolerance
Huntington Chorea
Lifespan
Nonhuman
Protein Aggregation
Protein Degradation
Protein Homeostasis
Protein Misfolding
Quantitative Analysis
Rna Interference
Sensory Nerve Cell
Stress
Alzheimer Disease
Animals
Drug Effect
Huntington Chorea
Metabolism
Paullinia
Alzheimer Disease
Animal
Antioxidants
Caenorhabditis Elegans
Huntington Disease
Paullinia
Plant Extracts
Data do documento: 2018
Revista: Oxidative Medicine and Cellular Longevity
É parte de: Volume 2018
Abstract: Guarana (Paullinia cupana) is largely consumed in Brazil in high energy drinks and dietary supplements because of its stimulant activity on the central nervous system. Although previous studies have indicated that guarana has some protective effects in Parkinson's (PD), Alzheimer's (AD), and Huntington's (HD) disease models, the underlying mechanisms are unknown. Here, we investigated the protective effects of guarana hydroalcoholic extract (GHE) in Caenorhabditis elegans models of HD and AD. GHE reduced polyglutamine (polyQ) protein aggregation in the muscle and also reduced polyQ-mediated neuronal death in ASH sensory neurons and delayed β-amyloid-induced paralysis in a caffeine-independent manner. Moreover, GHE's protective effects were not mediated by caloric restriction, antimicrobial effects, or development and reproduction impairment. Inactivation of the transcription factors SKN-1 and DAF-16 by RNAi partially blocked the protective effects of GHE treatment in the AD model. We show that the protective effect of GHE is associated with antioxidant activity and modulation of proteostasis, since it increased the lifespan and proteasome activity, reduced intracellular ROS and the accumulation of autophagosomes, and increased the expression of SOD-3 and HSP-16.2. Our findings suggest that GHE has therapeutic potential in combating age-related diseases associated with protein misfolding and accumulation. © 2018 Patrícia Ferreira Boasquívis et al.
DOI: 10.1155/2018/9241308
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