The effect of resveratrol on angiotensin II levels and the rate of transcription of its receptors in the rat cardiac hypertrophy model

Mashhadi, Fahimeh Dorri; Reza, Javad Zavvar; Jamhiri, Mohabbat; Hafizi, Zeinab; Mehrjardi, Fatemeh Zare; Safari, Fatemeh

doi:10.1007/s12576-016-0465-0

Cited by 19 publications

(8 citation statements)

References 34 publications

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“…Some investigations have also shown the anti-hypertrophic effects of resveratrol. For example, in our previous study, we reported that following hypertrophy induced by abdominal aortic banding in rat, resveratrol exerts antihypertrophic effects at a non-hypotensive dose, in part by normalizing AT1a mRNA levels (Mashhadi et al, 2017). Resveratrol exerts its antihypertrophic effect by decreasing protein synthesis and cellular growth due to phenylephrine in rat cardiac myocytes (Chan et al, 2008).…”

Section: Discussionmentioning

confidence: 96%

Resveratrol suppresses interleukin‐6 expression through activation of sirtuin 1 in hypertrophied H9c2 cardiomyoblasts

Akhondzadeh

Astani

Najjari

et al. 2020

Journal Cellular Physiology

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Inflammatory cytokine, interleukin-6 (IL-6), plays an important role in the pathogenesis of cardiac hypertrophy. Recent studies have documented that resveratrol exhibits cardioprotective effects. The present study attempts to explore whether resveratrol suppreses IL-6 in hypertrophied H9c2 cardiomyoblasts through histone deacetylase, sirtuin 1 (SIRT1). To induce hypertrophy, the cells were incubated with angiotensin II (Ang II). Treatment groups were treated with different doses (1, 10, 25, 50, 75, and 100 μM) of resveratrol (R). Cell viability was measured using 3-(4,5dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Cell size was determined using crystal violet staining. Gene expression was assessed by real-time polymerase chain reaction technique. Enzyme-linked immunosorbent assay was used to measure IL-6 concentration. The results showed that cell area and ANP messenger RNA (mRNA) levels decreased significantly in R25+Ang, R50+Ang, and R100+Ang groups, as compared with Ang group. Therefore, 10, 20, 30, 40, and 50 μM of resveratrol were used to to evaluate its anti-inflammatory effects. The results revealed that Ang II upregulated IL-6 at both mRNA and protein levels (p < .001 vs. normal) and resveratrol (50 μM) decreased IL-6 mRNA (p < .01) and protein (p < .05) significantly in comparison to Ang group. However, in groups in which the cells were pretreated with SIRT1 inhibitor, EX-527, the response of resveratrol was partially reversed. Transcription levels of IL-6 receptor components (gp130 and gp80) did not change significantly among the experimental groups. The current data suggests that resveratrol protects H9c2 cells against Ang II-induced hypertrophy by suppression of IL-6 through SIRT1 activation.

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Section: Discussionmentioning

confidence: 96%

Resveratrol suppresses interleukin‐6 expression through activation of sirtuin 1 in hypertrophied H9c2 cardiomyoblasts

Akhondzadeh

Astani

Najjari

et al. 2020

Journal Cellular Physiology

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“…Cardiac hypertrophy index (mg/g) was calculated from the total heart weight (mg) relative to total body weight (g) of the rat. 22…”

Section: Methodsmentioning

confidence: 99%

The Effects of Trimetazidine on QT-interval Prolongation and Cardiac Hypertrophy in Diabetic Rats

Ramezani-Aliakbari¹,

Badavi²,

Dianat³

et al. 2018

Arquivos Brasileiros De Cardiologia

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BackgroundTrimetazidine (TMZ) is an anti-ischemic drug. In spite of its protective effects on cardiovascular system, there is no scientific study on the usefulness of TMZ treatment for prolonged QT interval and cardiac hypertrophy induced by diabetes.ObjectivesTo evaluate the effects of TMZ on QT interval prolongation and cardiac hypertrophy in the diabetic rats.MethodsTwenty-four male Sprague-Dawley rats (200-250 g) were randomly assigned into three groups (n = 8) by simple random sampling method. Control (C), diabetic (D), and diabetic administrated with TMZ at 10 mg/kg (T10). TMZ was administrated for 8 weeks. The echocardiogram was recorded before isolating the hearts and transfer to a Langendorff apparatus. Hemodynamic parameters, QT and corrected QT interval (QTc) intervals, heart rate and antioxidant enzymes were measured. The hypertrophy index was calculated. The results were evaluated by one-way ANOVA and paired t-test using SPSS (version 16) and p < 0.05 was regarded as significant.ResultsThe diabetic rats significantly indicated increased hypertrophy, QT and QTc intervals and decreased Left ventricular systolic pressure (LVSP), Left ventricular developed pressure (LVDP), rate pressure product (RPP), Max dp/dt, and min dp/dt (±dp/dt max), heart rate, superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase in the heart. Treatment with TMZ in the diabetic animals was significantly improved these parameters in comparison to the untreated diabetic group.ConclusionsTMZ improves QTc interval prolongation and cardiac hypertrophy in diabetes.

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“…Resveratrol upregulates ACE2, increases Ang (1-7), stimulates Masreceptors, decreases Ang II levels and downregulates angiotensin-AT 1 receptor expression in the ageing kidney and also in animal models of cardiac hypertrophy (Dorri Mashhadi et al, 2017;Jang et al, 2018). Similar changes have been observed in aortic tissues of ageing animals where the drug exerted anti-inflammatory, anti-fibrotic and antioxidant actions (Kim et al, 2018).…”

Section: Resveratrolmentioning

confidence: 70%

Should ACE2 be given a chance in COVID-19 therapeutics: A semi-systematic review of strategies enhancing ACE2

Kaur

Acharya

Mondal

et al. 2020

European Journal of Pharmacology

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The severe acute respiratory syndrome corona virus-2 (SARS-CoV-2) has resulted in almost 28 million cases of COVID-19 (Corona virus disease-2019) and more than 900000 deaths worldwide since December 2019. In the absence of effective antiviral therapy and vaccine, treatment of COVID-19 is largely symptomatic. By making use of its spike (S) protein, the virus binds to its primary human cell receptor, angiotensin converting enzyme 2 (ACE2) which is present in the pulmonary epithelial cells as well as other organs. SARS-CoV-2 may cause a downregulation of ACE2. ACE2 plays a protective role in the pulmonary system through its Mas-receptor and alamandine-MrgD-TGR7 pathways. Loss of this protective effect could be a major component of COVID-19 pathogenesis. An attractive strategy in SARS-CoV-2 therapeutics would be to augment ACE2 either directly by supplementation or indirectly through drugs which increase its levels or stimulate its downstream players. In this semi-systematic review, we have analysed the pathophysiological interplay between ACE and ACE2 in the cardiopulmonary system, the modulation of these two proteins by SARS-CoV-2, and potential therapeutic avenues targeting ACE-Ang II and ACE2-Ang (1–7) axes, that can be utilized against COVID-19 disease progression.

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The effect of resveratrol on angiotensin II levels and the rate of transcription of its receptors in the rat cardiac hypertrophy model

Cited by 19 publications

References 34 publications

Resveratrol suppresses interleukin‐6 expression through activation of sirtuin 1 in hypertrophied H9c2 cardiomyoblasts

Resveratrol suppresses interleukin‐6 expression through activation of sirtuin 1 in hypertrophied H9c2 cardiomyoblasts

The Effects of Trimetazidine on QT-interval Prolongation and Cardiac Hypertrophy in Diabetic Rats

Should ACE2 be given a chance in COVID-19 therapeutics: A semi-systematic review of strategies enhancing ACE2

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