Carqueja (Baccharis trimera) Protects against Oxidative Stress andβ-Amyloid-Induced Toxicity inCaenorhabditis elegans

Paiva, Franciny Aparecida; Bonomo, L; Boasquivis, Patrícia Ferreira; Paula, Igor Thadeu Borges Raposo de; Guerra, Joyce Ferreira da Costa; Leal, Wagney Mendes; Silva, Marcelo Eustáquio; Pedrosa, Maria Lúcia; Oliveira, Riva de Paula

doi:10.1155/2015/740162

Cited by 22 publications

(19 citation statements)

References 68 publications

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“…Some authors have also explored the possible implication of JNK-1 in the polyphenols’ effects, as this transcription factor may also activate DAF-16 in parallel with the IIS pathway [ 124 ]. Studies with the jnk-1(gk7) mutant showed that the life prolonging effects of catechin [ 122 ] and quercetin [ 24 ], or the improvement in the resistance against oxidative stress of extracts from Açai ( Euterpe oleracea ) [ 142 ] or carqueja ( Baccharis trimera ) [ 143 ] were independent of JNK-1.…”

Section: Methodological Approaches For Antioxidants Evaluation In mentioning

confidence: 99%

Caenorhabditis elegans as a Model Organism to Evaluate the Antioxidant Effects of Phytochemicals

et al. 2020

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The nematode Caenorhabditis elegans was introduced as a model organism in biological research by Sydney Brenner in the 1970s. Since then, it has been increasingly used for investigating processes such as ageing, oxidative stress, neurodegeneration, or inflammation, for which there is a high degree of homology between C. elegans and human pathways, so that the worm offers promising possibilities to study mechanisms of action and effects of phytochemicals of foods and plants. In this paper, the genes and pathways regulating oxidative stress in C. elegans are discussed, as well as the methodological approaches used for their evaluation in the worm. In particular, the following aspects are reviewed: the use of stress assays, determination of chemical and biochemical markers (e.g., ROS, carbonylated proteins, lipid peroxides or altered DNA), influence on gene expression and the employment of mutant worm strains, either carrying loss-of-function mutations or fluorescent reporters, such as the GFP.

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Section: Methodological Approaches For Antioxidants Evaluation In mentioning

confidence: 99%

Caenorhabditis elegans as a Model Organism to Evaluate the Antioxidant Effects of Phytochemicals

et al. 2020

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“…RNA interference (RNAi) was performed using the feeding method described previously, with empty pL4440 as controls [ 27 ]. Briefly, RNAi clones were grown with 12.5 μ g/mL tetracycline and 100 μ g/mL ampicillin.…”

Section: Methodsmentioning

confidence: 99%

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

Boasquivis

Silva

Paiva

et al. 2018

Oxidative Medicine and Cellular Longevity

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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.

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“…Thus, the lifespan extension produced by quercetin-3-O-diglucoside in C. elegans was explained by upregulation of the genes daf-2, old-1, osr-1, and sek-1, whereas no modification was produced in the expression of daf-16, age-1, and sir-2.1 [12]. However, assays with a flavonol-rich extract obtained from Baccharis trimera concluded that the improvement in the stress resistance was independent of several stress-related signaling pathways (p38, JNK, and ERK) and transcription factors SKN-1 and DAF-16 [32].…”

Section: Q-rt-pcr Analysesmentioning

confidence: 99%

Exploring Target Genes Involved in the Effect of Quercetin on the Response to Oxidative Stress in Caenorhabditis elegans

et al. 2019

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Quercetin is one the most abundant flavonoids in the human diet. Although it is well known that quercetin exhibits a range of biological activities, the mechanisms behind these activities remain unresolved. The aim of this work is to progress in the knowledge of the molecular mechanisms involved in the biological effects of quercetin using Caenorhabditis elegans as a model organism. With this aim, the nematode has been used to explore the ability of this flavonoid to modulate the insulin/insulin-like growth factor 1(IGF-1) signaling pathway (IIS) and the expression of some genes related to stress response. Different methodological approaches have been used, i.e., assays in knockout mutant worms, gene expression assessment by RT-qPCR, and C. elegans transgenic strains expressing green fluorescent protein (GFP) reporters. The results showed that the improvement of the oxidative stress resistance of C. elegans induced by quercetin could be explained, at least in part, by the modulation of the insulin signaling pathway, involving genes age-1, akt-1, akt-2, daf-18, sgk-1, daf-2, and skn-1. However, this effect could be independent of the transcription factors DAF-16 and HSF-1 that regulate this pathway. Moreover, quercetin was also able to increase expression of hsp-16.2 in aged worms. This observation could be of particular interest to explain the effects of enhanced lifespan and greater resistance to stress induced by quercetin in C. elegans, since the expression of many heat shock proteins diminishes in aging worms.

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Carqueja (Baccharis trimera) Protects against Oxidative Stress andβ-Amyloid-Induced Toxicity inCaenorhabditis elegans

Cited by 22 publications

References 68 publications

Caenorhabditis elegans as a Model Organism to Evaluate the Antioxidant Effects of Phytochemicals

Caenorhabditis elegans as a Model Organism to Evaluate the Antioxidant Effects of Phytochemicals

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

Exploring Target Genes Involved in the Effect of Quercetin on the Response to Oxidative Stress in Caenorhabditis elegans

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