Comparing the Effects of Ferulic Acid and Sugarcane Aqueous Extract in In Vitro and In Vivo Neurotoxic Models

Aline Colonnello, Ilan Kotlar, María Eduarda de Lima, Alma Ortíz-Plata, Rodolfo García-Contreras, Félix Alexandre Antunes Soares, Michael Aschner, Abel Santamaría

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Molecules exhibiting antioxidant, neuroprotective, and regulatory properties inherent to natural products consumed by humans are gaining attention in biomedical research. Ferulic acid (FA) is a phenolic compound possessing antioxidant and cytoprotective properties. It is found in several vegetables, including sugarcane, where it serves as the main antioxidant component. Here, we compared the antioxidant and cytoprotective effects of FA with those of the total sugarcane aqueous extract (SCAE). Specifically, we assessed biochemical markers of cell dysfunction in rat cortical brain slices and markers of physiological stress in Caenorhabditis elegans upon exposure to toxins evoking different mechanisms of neurotoxicity, including direct oxidative stress and/or excitotoxicity. In rat cortical slices, FA (250 and 500 μM), but not SCAE (~ 270 μM of total polyphenols), prevented the loss of reductive capacity induced by the excitotoxin quinolinic acid (QUIN, 100 μM), the pro-oxidant agent ferrous sulfate (FeSO4, 25 μM), and the dopaminergic pro-oxidant 6-hydroxydopamine (6-OHDA, 100 μM). In wild-type (N2) C. elegans, FA (38 mM) exerted protective effects on decreased survival induced by FeSO4 (15 mM) and 6-OHDA (25 mM), and the motor alterations induced by QUIN (100 mM), FeSO4, and 6-OHDA. In contrast, SCAE (~ 13.5 mM of total polyphenols) evoked protective effects on the decreased survival induced by the three toxic agents, the motor alterations induced by FeSO4, and the reproductive deficit induced by FeSO4. In addition, FA was unable to reverse the decreased survival induced by all these toxins in the skn-1−/− strain (VC1772), which lacks the homolog of mammalian Nrf2, a master antioxidant gene. Altogether, our results suggest that (1) both FA and SCAE afford protection against toxic conditions, (2) not all the effects inherent to SCAE are due to FA, and (3) FA requires the skn-1 pathway to exert its protective effects in C. elegans.

Original languageEnglish (US)
Pages (from-to)1-9
Number of pages9
JournalNeurotoxicity Research
DOIs
StateAccepted/In press - Jun 15 2018

Fingerprint

ferulic acid
Saccharum
Oxidopamine
Antioxidants
Caenorhabditis elegans
ferrous sulfate
Poisons
Polyphenols
Rats
Reactive Oxygen Species
Quinolinic Acid
Physiological Stress
Oxidative stress
Survival
In Vitro Techniques
Neurotoxins
Vegetables
Biological Products

Keywords

  • Antioxidant defense
  • C. elegans
  • Ferulic acid
  • Neurotoxic models
  • Protective effects
  • Rat cortical slices
  • Sugarcane

ASJC Scopus subject areas

  • Neuroscience(all)
  • Toxicology

Cite this

Colonnello, A., Kotlar, I., de Lima, M. E., Ortíz-Plata, A., García-Contreras, R., Soares, F. A. A., ... Santamaría, A. (Accepted/In press). Comparing the Effects of Ferulic Acid and Sugarcane Aqueous Extract in In Vitro and In Vivo Neurotoxic Models. Neurotoxicity Research, 1-9. https://doi.org/10.1007/s12640-018-9926-y

Comparing the Effects of Ferulic Acid and Sugarcane Aqueous Extract in In Vitro and In Vivo Neurotoxic Models. / Colonnello, Aline; Kotlar, Ilan; de Lima, María Eduarda; Ortíz-Plata, Alma; García-Contreras, Rodolfo; Soares, Félix Alexandre Antunes; Aschner, Michael; Santamaría, Abel.

In: Neurotoxicity Research, 15.06.2018, p. 1-9.

Research output: Contribution to journalArticle

Colonnello, A, Kotlar, I, de Lima, ME, Ortíz-Plata, A, García-Contreras, R, Soares, FAA, Aschner, M & Santamaría, A 2018, 'Comparing the Effects of Ferulic Acid and Sugarcane Aqueous Extract in In Vitro and In Vivo Neurotoxic Models', Neurotoxicity Research, pp. 1-9. https://doi.org/10.1007/s12640-018-9926-y
Colonnello, Aline ; Kotlar, Ilan ; de Lima, María Eduarda ; Ortíz-Plata, Alma ; García-Contreras, Rodolfo ; Soares, Félix Alexandre Antunes ; Aschner, Michael ; Santamaría, Abel. / Comparing the Effects of Ferulic Acid and Sugarcane Aqueous Extract in In Vitro and In Vivo Neurotoxic Models. In: Neurotoxicity Research. 2018 ; pp. 1-9.
@article{891ef818d3704974a4da9a526e797ba7,
title = "Comparing the Effects of Ferulic Acid and Sugarcane Aqueous Extract in In Vitro and In Vivo Neurotoxic Models",
abstract = "Molecules exhibiting antioxidant, neuroprotective, and regulatory properties inherent to natural products consumed by humans are gaining attention in biomedical research. Ferulic acid (FA) is a phenolic compound possessing antioxidant and cytoprotective properties. It is found in several vegetables, including sugarcane, where it serves as the main antioxidant component. Here, we compared the antioxidant and cytoprotective effects of FA with those of the total sugarcane aqueous extract (SCAE). Specifically, we assessed biochemical markers of cell dysfunction in rat cortical brain slices and markers of physiological stress in Caenorhabditis elegans upon exposure to toxins evoking different mechanisms of neurotoxicity, including direct oxidative stress and/or excitotoxicity. In rat cortical slices, FA (250 and 500 μM), but not SCAE (~ 270 μM of total polyphenols), prevented the loss of reductive capacity induced by the excitotoxin quinolinic acid (QUIN, 100 μM), the pro-oxidant agent ferrous sulfate (FeSO4, 25 μM), and the dopaminergic pro-oxidant 6-hydroxydopamine (6-OHDA, 100 μM). In wild-type (N2) C. elegans, FA (38 mM) exerted protective effects on decreased survival induced by FeSO4 (15 mM) and 6-OHDA (25 mM), and the motor alterations induced by QUIN (100 mM), FeSO4, and 6-OHDA. In contrast, SCAE (~ 13.5 mM of total polyphenols) evoked protective effects on the decreased survival induced by the three toxic agents, the motor alterations induced by FeSO4, and the reproductive deficit induced by FeSO4. In addition, FA was unable to reverse the decreased survival induced by all these toxins in the skn-1−/− strain (VC1772), which lacks the homolog of mammalian Nrf2, a master antioxidant gene. Altogether, our results suggest that (1) both FA and SCAE afford protection against toxic conditions, (2) not all the effects inherent to SCAE are due to FA, and (3) FA requires the skn-1 pathway to exert its protective effects in C. elegans.",
keywords = "Antioxidant defense, C. elegans, Ferulic acid, Neurotoxic models, Protective effects, Rat cortical slices, Sugarcane",
author = "Aline Colonnello and Ilan Kotlar and {de Lima}, {Mar{\'i}a Eduarda} and Alma Ort{\'i}z-Plata and Rodolfo Garc{\'i}a-Contreras and Soares, {F{\'e}lix Alexandre Antunes} and Michael Aschner and Abel Santamar{\'i}a",
year = "2018",
month = "6",
day = "15",
doi = "10.1007/s12640-018-9926-y",
language = "English (US)",
pages = "1--9",
journal = "Neurotoxicity Research",
issn = "1029-8428",
publisher = "Springer New York",

}

TY - JOUR

T1 - Comparing the Effects of Ferulic Acid and Sugarcane Aqueous Extract in In Vitro and In Vivo Neurotoxic Models

AU - Colonnello, Aline

AU - Kotlar, Ilan

AU - de Lima, María Eduarda

AU - Ortíz-Plata, Alma

AU - García-Contreras, Rodolfo

AU - Soares, Félix Alexandre Antunes

AU - Aschner, Michael

AU - Santamaría, Abel

PY - 2018/6/15

Y1 - 2018/6/15

N2 - Molecules exhibiting antioxidant, neuroprotective, and regulatory properties inherent to natural products consumed by humans are gaining attention in biomedical research. Ferulic acid (FA) is a phenolic compound possessing antioxidant and cytoprotective properties. It is found in several vegetables, including sugarcane, where it serves as the main antioxidant component. Here, we compared the antioxidant and cytoprotective effects of FA with those of the total sugarcane aqueous extract (SCAE). Specifically, we assessed biochemical markers of cell dysfunction in rat cortical brain slices and markers of physiological stress in Caenorhabditis elegans upon exposure to toxins evoking different mechanisms of neurotoxicity, including direct oxidative stress and/or excitotoxicity. In rat cortical slices, FA (250 and 500 μM), but not SCAE (~ 270 μM of total polyphenols), prevented the loss of reductive capacity induced by the excitotoxin quinolinic acid (QUIN, 100 μM), the pro-oxidant agent ferrous sulfate (FeSO4, 25 μM), and the dopaminergic pro-oxidant 6-hydroxydopamine (6-OHDA, 100 μM). In wild-type (N2) C. elegans, FA (38 mM) exerted protective effects on decreased survival induced by FeSO4 (15 mM) and 6-OHDA (25 mM), and the motor alterations induced by QUIN (100 mM), FeSO4, and 6-OHDA. In contrast, SCAE (~ 13.5 mM of total polyphenols) evoked protective effects on the decreased survival induced by the three toxic agents, the motor alterations induced by FeSO4, and the reproductive deficit induced by FeSO4. In addition, FA was unable to reverse the decreased survival induced by all these toxins in the skn-1−/− strain (VC1772), which lacks the homolog of mammalian Nrf2, a master antioxidant gene. Altogether, our results suggest that (1) both FA and SCAE afford protection against toxic conditions, (2) not all the effects inherent to SCAE are due to FA, and (3) FA requires the skn-1 pathway to exert its protective effects in C. elegans.

AB - Molecules exhibiting antioxidant, neuroprotective, and regulatory properties inherent to natural products consumed by humans are gaining attention in biomedical research. Ferulic acid (FA) is a phenolic compound possessing antioxidant and cytoprotective properties. It is found in several vegetables, including sugarcane, where it serves as the main antioxidant component. Here, we compared the antioxidant and cytoprotective effects of FA with those of the total sugarcane aqueous extract (SCAE). Specifically, we assessed biochemical markers of cell dysfunction in rat cortical brain slices and markers of physiological stress in Caenorhabditis elegans upon exposure to toxins evoking different mechanisms of neurotoxicity, including direct oxidative stress and/or excitotoxicity. In rat cortical slices, FA (250 and 500 μM), but not SCAE (~ 270 μM of total polyphenols), prevented the loss of reductive capacity induced by the excitotoxin quinolinic acid (QUIN, 100 μM), the pro-oxidant agent ferrous sulfate (FeSO4, 25 μM), and the dopaminergic pro-oxidant 6-hydroxydopamine (6-OHDA, 100 μM). In wild-type (N2) C. elegans, FA (38 mM) exerted protective effects on decreased survival induced by FeSO4 (15 mM) and 6-OHDA (25 mM), and the motor alterations induced by QUIN (100 mM), FeSO4, and 6-OHDA. In contrast, SCAE (~ 13.5 mM of total polyphenols) evoked protective effects on the decreased survival induced by the three toxic agents, the motor alterations induced by FeSO4, and the reproductive deficit induced by FeSO4. In addition, FA was unable to reverse the decreased survival induced by all these toxins in the skn-1−/− strain (VC1772), which lacks the homolog of mammalian Nrf2, a master antioxidant gene. Altogether, our results suggest that (1) both FA and SCAE afford protection against toxic conditions, (2) not all the effects inherent to SCAE are due to FA, and (3) FA requires the skn-1 pathway to exert its protective effects in C. elegans.

KW - Antioxidant defense

KW - C. elegans

KW - Ferulic acid

KW - Neurotoxic models

KW - Protective effects

KW - Rat cortical slices

KW - Sugarcane

UR - http://www.scopus.com/inward/record.url?scp=85048578516&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85048578516&partnerID=8YFLogxK

U2 - 10.1007/s12640-018-9926-y

DO - 10.1007/s12640-018-9926-y

M3 - Article

SP - 1

EP - 9

JO - Neurotoxicity Research

JF - Neurotoxicity Research

SN - 1029-8428

ER -