Ellagic acid prevents myocardial infarction-induced left ventricular diastolic dysfunction in ovariectomized rats

Research output: Contribution to journalJournal articlepeer-review

Standard

Ellagic acid prevents myocardial infarction-induced left ventricular diastolic dysfunction in ovariectomized rats. / Costa, Bruno Maia; Mengal, Vinícius; Brasil, Girlandia Alexandre; Peluso, Antônio Augusto; Treebak, Jonas T.; Endlich, Patrick Wander; de Almeida, Simone Alves; de Abreu, Gláucia Rodrigues.

In: Journal of Nutritional Biochemistry, Vol. 105, 108990, 2022.

Research output: Contribution to journalJournal articlepeer-review

Harvard

Costa, BM, Mengal, V, Brasil, GA, Peluso, AA, Treebak, JT, Endlich, PW, de Almeida, SA & de Abreu, GR 2022, 'Ellagic acid prevents myocardial infarction-induced left ventricular diastolic dysfunction in ovariectomized rats', Journal of Nutritional Biochemistry, vol. 105, 108990. https://doi.org/10.1016/j.jnutbio.2022.108990

APA

Costa, B. M., Mengal, V., Brasil, G. A., Peluso, A. A., Treebak, J. T., Endlich, P. W., de Almeida, S. A., & de Abreu, G. R. (2022). Ellagic acid prevents myocardial infarction-induced left ventricular diastolic dysfunction in ovariectomized rats. Journal of Nutritional Biochemistry, 105, [108990]. https://doi.org/10.1016/j.jnutbio.2022.108990

Vancouver

Costa BM, Mengal V, Brasil GA, Peluso AA, Treebak JT, Endlich PW et al. Ellagic acid prevents myocardial infarction-induced left ventricular diastolic dysfunction in ovariectomized rats. Journal of Nutritional Biochemistry. 2022;105. 108990. https://doi.org/10.1016/j.jnutbio.2022.108990

Author

Costa, Bruno Maia ; Mengal, Vinícius ; Brasil, Girlandia Alexandre ; Peluso, Antônio Augusto ; Treebak, Jonas T. ; Endlich, Patrick Wander ; de Almeida, Simone Alves ; de Abreu, Gláucia Rodrigues. / Ellagic acid prevents myocardial infarction-induced left ventricular diastolic dysfunction in ovariectomized rats. In: Journal of Nutritional Biochemistry. 2022 ; Vol. 105.

Bibtex

@article{2d6f205f668d4192a0e1ff0c4920343f,
title = "Ellagic acid prevents myocardial infarction-induced left ventricular diastolic dysfunction in ovariectomized rats",
abstract = "Estrogen deficiency is associated with increased oxidative stress, which can contribute to left ventricular diastolic dysfunction (LVDD). We hypothesized that oral treatment with ellagic acid (EA), a potent and natural antioxidant compound, can improve MI-induced LVDD in ovariectomized rats, by reducing the formation of reactive oxygen species. Ovariectomized rats MI-induced LVDD followed by treatment with vehicle (DD) or EA (DD + EA) for 4 weeks. Non-LVDD-induced rats treated with vehicle (S) or EA (S + EA) were used as controls. Left ventricular systolic pressure; left ventricular end-diastolic pressure (LVEDP); maximum rate of pressure rise: +dP/dt and fall: –dP/dt) were evaluated in all animals after treatment. Left ventricle superoxide anion formation was quantified in situ by fluorescence. Phospho-CAMKII, SOD2, catalase, and gp91-phox abundances were evaluated by Western blot analyses. SOD (superoxide dismutase) and catalase activities were measured by spectrophotometry. The results showed that the LVEDP was significantly increased in both DD and DD + EA groups compared to S and S + EA. However, LVEDP in the DD + EA group was significantly decreased compared to DD, indicating an EA-mediated effect. In the DD group, superoxide production and gp91-phox protein abundance were increased while SOD2 abundance was decreased when compared to the S and S + EA groups. An increase in SOD activity was also observed in the DD + EA group. EA treatment reduced CaMKII phosphorylation in the DD + EA group compared to the DD. We concluded that EA treatment attenuated diastolic dysfunction in our experimental model, via reduction of reactive oxygen species and CaMKII activity, indicating EA as a promising natural therapeutic option for cardiac dysfunction.",
keywords = "Antioxidant Enzymes, Diastolic Heart Failure, Experimental Menopause, Oxidative Stress, Polyphenols",
author = "Costa, {Bruno Maia} and Vin{\'i}cius Mengal and Brasil, {Girlandia Alexandre} and Peluso, {Ant{\^o}nio Augusto} and Treebak, {Jonas T.} and Endlich, {Patrick Wander} and {de Almeida}, {Simone Alves} and {de Abreu}, {Gl{\'a}ucia Rodrigues}",
note = "Publisher Copyright: {\textcopyright} 2022 Elsevier Inc.",
year = "2022",
doi = "10.1016/j.jnutbio.2022.108990",
language = "English",
volume = "105",
journal = "Journal of Nutritional Biochemistry",
issn = "0955-2863",
publisher = "Elsevier",

}

RIS

TY - JOUR

T1 - Ellagic acid prevents myocardial infarction-induced left ventricular diastolic dysfunction in ovariectomized rats

AU - Costa, Bruno Maia

AU - Mengal, Vinícius

AU - Brasil, Girlandia Alexandre

AU - Peluso, Antônio Augusto

AU - Treebak, Jonas T.

AU - Endlich, Patrick Wander

AU - de Almeida, Simone Alves

AU - de Abreu, Gláucia Rodrigues

N1 - Publisher Copyright: © 2022 Elsevier Inc.

PY - 2022

Y1 - 2022

N2 - Estrogen deficiency is associated with increased oxidative stress, which can contribute to left ventricular diastolic dysfunction (LVDD). We hypothesized that oral treatment with ellagic acid (EA), a potent and natural antioxidant compound, can improve MI-induced LVDD in ovariectomized rats, by reducing the formation of reactive oxygen species. Ovariectomized rats MI-induced LVDD followed by treatment with vehicle (DD) or EA (DD + EA) for 4 weeks. Non-LVDD-induced rats treated with vehicle (S) or EA (S + EA) were used as controls. Left ventricular systolic pressure; left ventricular end-diastolic pressure (LVEDP); maximum rate of pressure rise: +dP/dt and fall: –dP/dt) were evaluated in all animals after treatment. Left ventricle superoxide anion formation was quantified in situ by fluorescence. Phospho-CAMKII, SOD2, catalase, and gp91-phox abundances were evaluated by Western blot analyses. SOD (superoxide dismutase) and catalase activities were measured by spectrophotometry. The results showed that the LVEDP was significantly increased in both DD and DD + EA groups compared to S and S + EA. However, LVEDP in the DD + EA group was significantly decreased compared to DD, indicating an EA-mediated effect. In the DD group, superoxide production and gp91-phox protein abundance were increased while SOD2 abundance was decreased when compared to the S and S + EA groups. An increase in SOD activity was also observed in the DD + EA group. EA treatment reduced CaMKII phosphorylation in the DD + EA group compared to the DD. We concluded that EA treatment attenuated diastolic dysfunction in our experimental model, via reduction of reactive oxygen species and CaMKII activity, indicating EA as a promising natural therapeutic option for cardiac dysfunction.

AB - Estrogen deficiency is associated with increased oxidative stress, which can contribute to left ventricular diastolic dysfunction (LVDD). We hypothesized that oral treatment with ellagic acid (EA), a potent and natural antioxidant compound, can improve MI-induced LVDD in ovariectomized rats, by reducing the formation of reactive oxygen species. Ovariectomized rats MI-induced LVDD followed by treatment with vehicle (DD) or EA (DD + EA) for 4 weeks. Non-LVDD-induced rats treated with vehicle (S) or EA (S + EA) were used as controls. Left ventricular systolic pressure; left ventricular end-diastolic pressure (LVEDP); maximum rate of pressure rise: +dP/dt and fall: –dP/dt) were evaluated in all animals after treatment. Left ventricle superoxide anion formation was quantified in situ by fluorescence. Phospho-CAMKII, SOD2, catalase, and gp91-phox abundances were evaluated by Western blot analyses. SOD (superoxide dismutase) and catalase activities were measured by spectrophotometry. The results showed that the LVEDP was significantly increased in both DD and DD + EA groups compared to S and S + EA. However, LVEDP in the DD + EA group was significantly decreased compared to DD, indicating an EA-mediated effect. In the DD group, superoxide production and gp91-phox protein abundance were increased while SOD2 abundance was decreased when compared to the S and S + EA groups. An increase in SOD activity was also observed in the DD + EA group. EA treatment reduced CaMKII phosphorylation in the DD + EA group compared to the DD. We concluded that EA treatment attenuated diastolic dysfunction in our experimental model, via reduction of reactive oxygen species and CaMKII activity, indicating EA as a promising natural therapeutic option for cardiac dysfunction.

KW - Antioxidant Enzymes

KW - Diastolic Heart Failure

KW - Experimental Menopause

KW - Oxidative Stress

KW - Polyphenols

U2 - 10.1016/j.jnutbio.2022.108990

DO - 10.1016/j.jnutbio.2022.108990

M3 - Journal article

C2 - 35331902

AN - SCOPUS:85128449033

VL - 105

JO - Journal of Nutritional Biochemistry

JF - Journal of Nutritional Biochemistry

SN - 0955-2863

M1 - 108990

ER -

ID: 305186645