Guarana (Paullinia cupana) Extract Protects Caenorhabditis elegans Models for Alzheimer Disease and Huntington Disease through Activation of Antioxidant and Protein Degradation Pathways

• Autor(a) principal: Boasquívis, Patrícia Ferreira
• Data de Publicação: 2018
• Outros Autores: Silva, Giovanna Melo Martins, Paiva, Franciny Aparecida, Cavalcanti, Rodrigo Marinho, Nunez, C. V., Paula Oliveira, Riva de
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Institucional do INPA
• Texto Completo: https://repositorio.inpa.gov.br/handle/1/15675
• topic: 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

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.