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

Autor: Costa BM; Department of Physiological Sciences, Health Sciences Center, Federal University of Espírito Santo, Vitória, Espírito Santo, Brazil., Mengal V; Department of Physiological Sciences, Health Sciences Center, Federal University of Espírito Santo, Vitória, Espírito Santo, Brazil., Brasil GA; Department of Pharmacy, University Vila Velha, Vila Velha, Espírito Santo, Brazil., Peluso AA; Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark., Treebak JT; Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark., Endlich PW; Faculdade de Medicina do Mucuri, Multicentric Post-Graduate Program in Physiological Sciences, Universidade Federal dos Vales do Jequitinhonha e Mucuri, Teófilo Otoni, Minas Gerais, Brazil., de Almeida SA; Department of Physiological Sciences, Health Sciences Center, Federal University of Espírito Santo, Vitória, Espírito Santo, Brazil. Electronic address: simonealvesalmeida18@gmail.com., de Abreu GR; Department of Physiological Sciences, Health Sciences Center, Federal University of Espírito Santo, Vitória, Espírito Santo, Brazil.
Jazyk: angličtina
Zdroj: The Journal of nutritional biochemistry [J Nutr Biochem] 2022 Jul; Vol. 105, pp. 108990. Date of Electronic Publication: 2022 Mar 21.
DOI: 10.1016/j.jnutbio.2022.108990
Abstrakt: 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.
(Copyright © 2022 Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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