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J Nutr Biochem. 2016 Aug;34:106-17. doi: 10.1016/j.jnutbio.2016.05.004. Epub 2016 May 27.

Sulforaphane effects on postinfarction cardiac remodeling in rats: modulation of redox-sensitive prosurvival and proapoptotic proteins.

Author information

1
Laboratory of Cardiovascular Physiology, Institute of Basic Health Science, Federal University of Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil.
2
Laboratory of Cardiovascular Physiology, Institute of Basic Health Science, Federal University of Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil; Centro Universitário Ritter dos Reis (Uniritter), Porto Alegre, Rio Grande do Sul, Brazil.
3
Laboratório de Histofisiologia Comparada, Departamento de Ciências Morfológicas, Instituto de Ciências Básicas da Saúde, Federal University of Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil.
4
Laboratório de Biologia Celular e Tecidual, Departamento de Ciências Morfofisiológicas, Faculdade de Biociências, Pontifícia Universidade Católica do Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil.
5
Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, Winnipeg, Manitoba, Canada.
6
Medical Sciences Division, Northern Ontario School of Medicine, Lakehead University, Thunder Bay, Ontario, Canada.
7
Laboratory of Cardiovascular Physiology, Institute of Basic Health Science, Federal University of Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil. Electronic address: belklein@ufrgs.br.

Abstract

This study investigated whether sulforaphane (SFN), a compound found in cruciferous vegetables, could attenuate the progression of post-myocardial infarction (MI) cardiac remodeling. Male Wistar rats (350 g) were allocated to four groups: SHAM (n=8), SHAM+SFN (n=7), MI (n=8) and MI+SFN (n=5). On the third day after surgery, cardiac function was assessed and SFN treatment (5 mg/kg/day) was started. At the end of 25 days of treatment, cardiac function was assessed and heart was collected to measure collagen content, oxidative stress and protein kinase. MI and MI+SFN groups presented cardiac dysfunction, without signs of congestion. Sulforaphane reduced fibrosis (2.1-fold) in infarcted rats, which was associated with a slight attenuation in the cardiac remodeling process. Both infarcted groups presented increases in the oxidative markers xanthine oxidase and 4-hydroxinonenal, as well as a parallel increase in the antioxidant enzymes glutathione peroxidase and superoxide dismutase. Moreover, sulforaphane stimulated the cytoprotective heme oxygenase-1 (HO-1) (38%). Oxidative markers correlated with ERK 1/2 activation. In the MI+SFN group, up-regulation of ERK 1/2 (34%) and Akt (35%), as well as down-regulation of p38 (52%), was observed. This change in the prosurvival kinase balance in the MI+SFN group was related to a down-regulation of apoptosis pathways (Bax/Bcl-2/caspase-3). Sulforaphane was unable to modulate autophagy. Taken together, sulforaphane increased HO-1, which may generate a redox environment in the cardiac tissue favorable to activation of prosurvival and deactivation of prodeath pathways. In conclusion, this natural compound contributes to attenuation of the fibrotic process, which may contribute to mitigation against the progression of cardiac remodeling postinfarction.

KEYWORDS:

Autophagy; Heart failure; Heme oxygenase-1; Isothiocyanate; Myocardial infarction; Oxidative stress

PMID:
27288935
DOI:
10.1016/j.jnutbio.2016.05.004
[Indexed for MEDLINE]

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