Improving overall health and quality of life, preventing diseases and increasing life expectancy are key concerns in the field of public health. The search for antioxidants that can inhibit oxidative damage in cells has received a lot of attention. Rosmarinus officinalis L. represents an exceptionally rich source of bioactive compounds with pharmacological properties. In the present study, we explored the effects of the ethanolic extract of R. officinalis (eeRo) on stress resistance and longevity using the non-parasitic nematode Caenorhabditis elegans as a model. We report for the first time that eeRo increased resistance against oxidative and thermal stress and extended C. elegans longevity in an insulin/IGF signaling pathway-dependent manner. These data emphasize the eeRo beneficial effects on C. elegans under stress.
Quinolinic acid (QUIN) is an endogenous neurotoxin that acts as an N-methyl-D-aspartate receptor (NMDAR) agonist generating a toxic cascade, which can lead to neurodegeneration. The action of QUIN in Caenorhabditis elegans and the neurotoxins that allow the study of glutamatergic system disorders have not been carefully addressed. The effects of QUIN on toxicological and behavioral parameters in VM487 and VC2623 transgenic, as well as wild-type (WT) animals were performed to evaluate whether QUIN could be used as a neurotoxin in C. elegans. QUIN reduced survival of WT worms in a dose-dependent manner. A sublethal dose of QUIN (20 mM) increased reactive oxygen species (ROS) levels in an nmr-1/NMDAR-dependent manner, activated the DAF-16/FOXO transcription factor, and increased expression of the antioxidant enzymes, superoxide dismutase-3, glutathione S-transferase-4, and heat shock protein-16.2. QUIN did not change motor behavioral parameters, but altered the sensory behavior in N2 and VM487 worms. Notably, the effect of QUIN on the sensory behavioral parameters might occur, at least in part, secondary to increased ROS. However, the touch response behavior indicates a mechanism of action that is independent of ROS generation. In addition, non-lethal doses of QUIN triggered neurodegeneration in glutamatergic neurons. Our findings indicate that C. elegans might be useful as a model for studies of QUIN as a glutamatergic neurotoxin in rodent models.
Guarana (Paullinia cupana) is habitually ingested by people in
the Amazon region and is a key ingredient in various energy drinks consumed
worldwide. Extension in longevity and low prevalence of chronic age-related
diseases have been associated to habitual intake of guarana. Anti-aging
potential of guarana was also demonstrated in Caenorhabditis
elegans; however, the mechanisms involved in its effects are not
clear. Herein, we investigated the putative pathways that regulate the effects
of guarana ethanolic extract (GEE) on lifespan using C.
elegans. The major known longevity pathways were analyzed through
mutant worms and RT-qPCR assay (DAF-2, DAF-16, SKN-1, SIR-2.1, HSF-1). The
possible involvement of purinergic signaling was also investigated. This study
demonstrated that GEE acts through antioxidant activity, DAF-16, HSF-1, and
SKN-1 pathways, and human adenosine receptor ortholog (ADOR-1) to extend
lifespan. GEE also downregulated skn-1,
daf-16, sir-2.1 and hsp-16.2
in 9-day-old C. elegans, which might reflect less need to
activate these protective genes due to direct antioxidant effects. Our results
contribute to the comprehension of guarana effects in vivo,
which might be helpful to prevent or treat aging-associated disorders, and also
suggest purinergic signaling as a plausible therapeutic target for longevity
studies.
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