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

Fernandes, Rafael Oliveira; Castro, Alexandre Luz de; Bonetto, Jéssica Hellen Poletto; Ortiz, Vanessa Duarte; Muller, Dalvana Daneliza; Carraro, Cristina Campos; Barbosa, Sílvia; Neves, Laura Tartari; Xavier, Léder Leal; Schenkel, Paulo Cavalheiro; Singal, Pawan K.; Khaper, Neelam; Araújo, Alex Sander da Rosa

doi:10.1016/j.jnutbio.2016.05.004

Cited by 29 publications

(26 citation statements)

References 62 publications

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“…Therefore, we suggest that SFN may improve urinary function, not by restraining muscle cell apoptosis, but by preserving muscle function. Similar to other reported studies [29] [40], SFN could improve muscle contractile function, preserve the normal muscle morphology, protect muscles from oxidative damage, and decrease collagen expression. The precise mechanism through which SFN influences the urethral sphincter muscle should be further explored.…”

Section: Discussionsupporting

confidence: 89%

Sulforaphane Treatment of Stress Urinary Incontinence Via the Nrf2-ARE Pathway in a Rat Model

Wan¹,

Liu²,

Chen³

et al. 2017

Cell Physiol Biochem

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Background/Aims: To explore the effect of sulforaphane (SFN) treatment in rats through the induction of Stress Urinary Incontinence (SUI) via the Nrf2-ARE pathway. Methods: A total of 18 female rats (Sprague-Dawley) were assigned to three groups: a control group, an SUI group, and an SUI+SFN group (six rats per group). Rats in the treatment groups were induced via postpartum vaginal balloon dilation and bilateral ovariectomy. Rats in the SUI+SFN group were treated via intraperitoneal injection once per day for a total of one month. Urethral sphincter muscle histological was observed by HE and Masson staining. Peak voiding pressure and interval of micturition were measured by cystometry. Oxidative stress markers and protein expression in the Nrf2-ARE pathway were examined by immunohistochemical staining and western blotting. Results: Prolonged micturition interval and higher peak voiding pressure were observed in the SUI+SFN group. Disturbance of muscle morphology was ameliorated, muscle content was elevated, and collagen content was restrained in response to SFN treatment. The SOD, GSH-Px, and CAT activities were elevated in the SUI+SFN group compared to those in the control group. The level of cell apoptosis was decreased in SUI rats after SFN treatment; however, apoptosis was mainly located in the urethral mucosa instead of the muscle layer. SFN reduced the Bax/Bcl-2 expression ratio. Nrf2 and Nrf2 target antioxidant proteins were elevated in the SFN group. Conclusions: SFN was effective for SUI treatment via decreasing oxidative stress and activating the Nrf2-ARE pathway.

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Section: Discussionsupporting

confidence: 89%

Sulforaphane Treatment of Stress Urinary Incontinence Via the Nrf2-ARE Pathway in a Rat Model

Wan¹,

Liu²,

Chen³

et al. 2017

Cell Physiol Biochem

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“…Studies have shown that SFN has pharmacological effects on the reduction of fibrosis, oxidative stress, and inflammation. Fernandes et al have shown that SFN reduced the rate of progression of cardiac remodeling post-infarction through its effects on reducing cardiac fibrosis and oxidative stress [ 11 ]. Other research groups have shown that SFN activates the transcriptional cofactor, PPAR-gamma coactivator 1-alpha (PGC1-α), which may be a mechanism by which SFN reduces oxidative stress and cell apoptosis [ 22 ].…”

Section: Discussionmentioning

confidence: 99%

“…Sulforaphane (SFN), is a natural isothiocyanate compound that is found in cruciferous vegetables, such as broccoli, cabbage, and cauliflower and is an antioxidant that has been shown to stimulate the production of intracellular antioxidants as well as phase-II detoxification enzymes [ 10 ]. The anti-oxidant effects of SFN have been shown to have a role in the prevention of the progression of chronic diseases of the cardiovascular system, kidney, brain, and also in cancer [ 11 – 14 ]. For example, SFN has been shown to be beneficial in the prevention of diabetes-induced cardiomyopathy by reducing cardiac fibrosis, oxidative stress, and inflammation, and has been shown to upregulate the expression of Nrf2 which provides cellular defense against oxidation [ 15 ].…”

Section: Introductionmentioning

confidence: 99%

Sulforaphane, a Natural Isothiocyanate Compound, Improves Cardiac Function and Remodeling by Inhibiting Oxidative Stress and Inflammation in a Rabbit Model of Chronic Heart Failure

Decai

Chen

et al. 2018

Med Sci Monit

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BackgroundThe aim of this study was to investigate the effects of sulforaphane (SFN), a natural isothiocyanate compound, in a rabbit ascending aortic cerclage model of chronic heart failure (CHF).Material/MethodsThirty New Zealand White rabbits were divided into the sham operation group (n=10), the CHF group (n=10), and the CHF + SFN group (n=10) treated with subcutaneous SFN (0.5 mg/kg) for five days per week for 12 weeks. After 12 weeks, echocardiography and biometric analysis were performed, followed by the examination of the rabbit hearts. Enzyme-linked immunosorbent assay (ELISA) and Western blot were used to detect levels of inflammatory cytokines, superoxide dismutase (SOD), and malondialdehyde (MDA).ResultsIn the CHF group, compared with the sham operation group, there was an increase in the heart weight to body weight ratio (HW/BW), the left ventricular weight to body weight ratio (LVW/BW), the left ventricular end diastolic diameter (LVEDD), the left ventricular end systolic diameter (LVESD), plasma brain natriuretic peptide (BNP) and atrial natriuretic peptide (ANP) levels, the cardiac collagen volume fraction (CVF), apoptotic index, expression levels of collagen I, collagen III, tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and malondialdehyde (MDA) in the myocardial tissue, and a decrease in the left ventricular shortening fraction (LVFS) and left ventricular ejection fraction (LVEF), and cardiac superoxide dismutase (SOD) activity. These changes were corrected in the SFN-treated group.ConclusionsIn a rabbit model of CHF, treatment with SFN improved cardiac function and remodeling by inhibiting oxidative stress and inflammation.

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“…In fact, accumulating study has paid great attention to drugs on anti-MF therapy through in vitro and in vivo experiments. Studies have shown that some drugs or plant extracts can inhibit MF through autophagy regulation, as well as reducing myocardial damage and improving cardiac function [ 22 , 77 , 78 ]. Promoting or suppressing autophagy all can achieve the purpose of inhibiting MF and ameliorating heart function, respectively, concluded from different studies.…”

Section: Potential Effect Of Autophagy In the Treatment Of Myocardmentioning

confidence: 99%

An Intervention Target for Myocardial Fibrosis: Autophagy

Yang

Zhu

et al. 2018

BioMed Research International

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Myocardial fibrosis (MF) is the result of metabolic imbalance of collagen synthesis and metabolism, which is widespread in various cardiovascular diseases. Autophagy is a lysosomal degradation pathway which is highly conserved. In recent years, research on autophagy has been increasing and the researchers have also become cumulatively aware of the specified association between autophagy and MF. This review highlights the role of autophagy in MF and the potential effects through the administration of medicine.

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

Cited by 29 publications

References 62 publications

Sulforaphane Treatment of Stress Urinary Incontinence Via the Nrf2-ARE Pathway in a Rat Model

Sulforaphane Treatment of Stress Urinary Incontinence Via the Nrf2-ARE Pathway in a Rat Model

Sulforaphane, a Natural Isothiocyanate Compound, Improves Cardiac Function and Remodeling by Inhibiting Oxidative Stress and Inflammation in a Rabbit Model of Chronic Heart Failure

An Intervention Target for Myocardial Fibrosis: Autophagy

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