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Guarana ( Paullinia cupana Mart.) Prevents β‐Amyloid Aggregation, Generation of Advanced Glycation‐end Products (AGEs), and Acrolein‐Induced Cytotoxicity on Human Neuronal‐Like Cells
Author(s) -
Bittencourt Leonardo da Silva,
ZeidánChuliá Fares,
Yatsu Francini Kiyono Jorge,
Schnorr Carlos Eduardo,
Moresco Karla Suzana,
Kolling Eduardo Antônio,
Gelain Daniel Pens,
Bassani Valquiria Linck,
Moreira José Cláudio Fonseca
Publication year - 2014
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.5173
Subject(s) - methylglyoxal , glycation , acrolein , pharmacology , chemistry , programmed cell death , biochemistry , medicine , apoptosis , enzyme , receptor , catalysis
Advanced glycation end‐products (AGEs) are considered potent molecules capable of promoting neuronal cell death and participating in the development of neurodegenerative disorders such as Alzheimer's disease (AD). Previous studies have shown that AGEs exacerbate β‐amyloid (Aβ) aggregation and AGE‐related cross‐links are also detected in senile plaques. Acrolein (ACR) is an α, β‐unsaturated aldehyde found in the environment and thermally processed foods, which can additionally be generated through endogenous metabolism. The role of ACR in AD is widely accepted in the literature. Guarana ( Paullinia cupana Mart.) is popularly consumed by the population in Brazil, mainly for its stimulant activity. In the present study, we showed that guarana (10, 100, and 1000 µg/mL) is able to prevent protein glycation, β‐amyloid aggregation, in vitro methylglyoxal, glyoxal, and ACR (20 μM)‐induced toxicity on neuronal‐like cells (SH‐SY5Y). Since these are considered typical AD pathological hallmarks, we propose that guarana may deserve further research as a potential therapeutic agent in such a neurodegenerative disease. Copyright © 2014 John Wiley & Sons, Ltd.