N-Acetylcysteine Influence on Oxidative Stress and Cardiac Remodeling in Rats During Transition from Compensated Left Ventricular Hypertrophy to Heart Failure

Reyes, David Rafael Abreu; Gomes, Mariana Janini; Rosa, Carlos J. P.; Pagan, Luana Urbano; Damatto, F C; Damatto, Ricardo Luiz; Deprá, Igor C.; Campos, Dijon Henrique Salomé de; Fernández, Ana Arpa; Martinez, Paula Felippe; Okoshi, Katashi; Okoshi, Marina Politi

doi:10.1159/000486115

Cited by 37 publications

(22 citation statements)

References 48 publications

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“…Since mitogen‐activated protein kinases (MAPK) may be involved in myocardial response to oxidative stress, we also evaluated their proteins expression in myocardium. Results for myocardial morphometric evaluation, oxidative stress analyses and protein expression from Sham and AS rats have been previously published …”

Section: Introductionmentioning

confidence: 99%

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Exercise during transition from compensated left ventricular hypertrophy to heart failure in aortic stenosis rats

Reyes

Gomes

Rosa

et al. 2018

J Cellular Molecular Medi

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We evaluated the influence of aerobic exercise on cardiac remodelling during the transition from compensated left ventricular (LV) hypertrophy to clinical heart failure in aortic stenosis (AS) rats. Eighteen weeks after AS induction, rats were assigned into sedentary (AS) and exercised (AS‐Ex) groups. Results were compared to Sham rats. Exercise was performed on treadmill for 8 weeks. Exercise improved functional capacity. Echocardiogram showed no differences between AS‐Ex and AS groups. After exercise, fractional shortening and ejection fraction were lower in AS‐Ex than Sham. Myocyte diameter and interstitial collagen fraction were higher in AS and AS‐Ex than Sham; however, myocyte diameter was higher in AS‐Ex than AS. Myocardial oxidative stress, evaluated by lipid hydroperoxide concentration, was higher in AS than Sham and was normalized by exercise. Gene expression of the NADPH oxidase subunits NOX2 and NOX4, which participate in ROS generation, did not differ between groups. Activity of the antioxidant enzyme superoxide dismutase was lower in AS and AS‐Ex than Sham and glutathione peroxidase was lower in AS‐Ex than Sham. Total and reduced myocardial glutathione, which is involved in cellular defence against oxidative stress, was lower in AS than Sham and total glutathione was higher in AS‐Ex than AS. The MAPK JNK was higher in AS‐Ex than Sham and AS groups. Phosphorylated P38 was lower in AS‐Ex than AS. Despite improving functional capacity, aerobic exercise does not change LV function in AS rats. Exercise restores myocardial glutathione, reduces oxidative stress, impairs JNK signalling and further induces myocyte hypertrophy.

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Section: Introductionmentioning

confidence: 99%

“…Results for myocardial morphometric evaluation, oxidative stress analyses and protein expression from Sham and AS rats have been previously published. 27…”

mentioning

confidence: 99%

Exercise during transition from compensated left ventricular hypertrophy to heart failure in aortic stenosis rats

Reyes

Gomes

Rosa

et al. 2018

J Cellular Molecular Medi

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“…cytochrome c oxidase subunit I) [161,305]Platelet-derivedgrowth factor receptor beta [272]Carnosine [283,286,288]Serine/threonine-protein kinase STK11 [309]Glutathione [260]Ether-a-go-go-related channels [310]Lipid peroxidation-derived aldehydesMDA Free MDA : Spectrophotometric methods (sample derivatization with TBA) [170,[172], [173], [174]] MDA-protein adducts : Spectrophotometric methods (sample derivatization with TBA, strong acids, hydrazine-based or non-hydrazine-based reagents) [171,180,183] LC-UV or LC-FD [176,177,180] LC-MS/MS (e.g. SRM/MRM MS or label-free ; sample derivatization with AIDA assay, 4-APC) [[186], [187], [188],194,195] GC-MS/MS (sample derivatization with hydrazine-based or non-hydrazine-based reagents) [178,179,190,191,196] CE-UV [193]Atherosclerosis [112]Coronary and peripheral artery disease [196,311]Aortic stenosis [265]Heart failure [312]Apolipoprotein B-100 (LDLs) [43]Apolipoprotein AI (HDLs) [313]Mitochondrial proteins [314]Carnosine [282,285]Lipid peroxidation-derived aldehydesACR Free ACR : Fluorescence methods (e.g. Skraup reaction with m-aminophenol, lanthanide probe) [202,204,205]LC-FD [206,208]LC-MS/MS (sample derivatization) [214] ACR-protein adducts : Immunochemical methods [209,…”

Section: Methods For Identification and Quantitation Of Lipid Peroxidmentioning

confidence: 99%

“…Indeed, a recent systematic review highlighted the ameliorative properties of NAC in preventing diabetes-induced cardiac damage through inhibition of oxidative stress [264], together with several preclinical studies supporting this effect. Reyes et al demonstrated in a rat model of long-term ascending aortic stenosis NAC treatment resulted in a reduction of myocardial fibrosis during the transition from compensated left ventricular (LV) hypertrophy to heart failure, paralleled by reduced oxidative stress due to restored glutathione levels and reduced MDA [265]. Giam et al demonstrated that NAC could blunt cardiac fibrosis and related remodeling in the setting of heart failure, in mice with cardiomyopathy secondary to the cardiac-specific overexpression of mammalian sterile 20‐like kinase 1, and this effect was ascribed to reduced oxidative stress [266].…”

Section: Molecular Strategies To Prevent Ales Formation In the Cardiomentioning

confidence: 99%

Lipoxidation in cardiovascular diseases

et al. 2019

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Lipids can go through lipid peroxidation, an endogenous chain reaction that consists in the oxidative degradation of lipids leading to the generation of a wide variety of highly reactive carbonyl species (RCS), such as short-chain carbonyl derivatives and oxidized truncated phospholipids. RCS exert a wide range of biological effects due to their ability to interact and covalently bind to nucleophilic groups on other macromolecules, such as nucleic acids, phospholipids, and proteins, forming reversible and/or irreversible modifications and generating the so-called advanced lipoxidation end-products (ALEs).Lipoxidation plays a relevant role in the onset of cardiovascular diseases (CVD), mainly in the atherosclerosis-based diseases in which oxidized lipids and their adducts have been extensively characterized and associated with several processes responsible for the onset and development of atherosclerosis, such as endothelial dysfunction and inflammation.Herein we will review the current knowledge on the sources of lipids that undergo oxidation in the context of cardiovascular diseases, both from the bloodstream and tissues, and the methods for detection, characterization, and quantitation of their oxidative products and protein adducts.Moreover, lipoxidation and ALEs have been associated with many oxidative-based diseases, including CVD, not only as potential biomarkers but also as therapeutic targets. Indeed, several therapeutic strategies, acting at different levels of the ALEs cascade, have been proposed, essentially blocking ALEs formation, but also their catabolism or the resulting biological responses they induce. However, a deeper understanding of the mechanisms of formation and targets of ALEs could expand the available therapeutic strategies.

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“…Hematoxylin and eosin-stained slides from LV tissue were used to measure approximately 50 cardiomyocyte diameters as the lower distance between myocyte borders drawn across the nucleus [24–26].…”

Section: Methodsmentioning

confidence: 99%

Influence of intermittent fasting on myocardial infarction-induced cardiac remodeling

Okoshi

Cezar

Polin

et al. 2019

BMC Cardiovasc Disord

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Background Information on the role of intermittent fasting (IF) on pathologic cardiac remodeling is scarce. We compared the effects of IF before and after myocardial infarction (MI) on rat cardiac remodeling and survival. Methods Wistar rats were intermittently fasted (food available every other day) or fed ad libitum for 12 weeks and then divided into three groups: AL – fed ad libitum; AL/IF - fed AL before MI and IF after MI; and IF – fed IF before and after MI. Echocardiogram was performed before MI and 2 and 12 weeks after surgery. Isolated hearts were evaluated in Langendorff preparations. Results Before surgery, body weight (BW) was lower in IF than AL. Final BW was lower in AL/IF and IF than AL. Perioperative mortality did not change between AL (31.3%) and IF (27.3%). Total mortality was lower in IF than AL. Before surgery, echocardiographic parameters did not differ between groups. Two weeks after surgery, MI size did not differ between groups. Twelve weeks after MI, left ventricular (LV) diastolic posterior wall thickness was lower in AL/IF and IF than AL. The percentage of variation of echocardiographic parameters between twelve and two weeks showed that MI size decreased in all groups and the reduction was higher in IF than AL/IF. In Langendorff preparations, LV volume at zero end-diastolic pressure (V0; AL: 0.41 ± 0.05; AL/IF: 0.34 ± 0.06; IF: 0.28 ± 0.05 mL) and at 25 mmHg end-diastolic pressure (V25; AL: 0.61 ± 0.05; AL/IF: 0.54 ± 0.07; IF: 0.44 ± 0.06 mL) was lower in AL/IF and IF than AL and V25 was lower in IF than AL/IF. V0/BW ratio was lower in IF than AL and LV weight/V0 ratio was higher in IF than AL. Myocyte diameter was lower in AL/IF and IF than AL (AL: 17.3 ± 1.70; AL/IF: 15.1 ± 2.21; IF: 13.4 ± 1.49 μm). Myocardial hydroxyproline concentration and gene expression of ANP, Serca 2a, and α- and β-myosin heavy chain did not differ between groups. Conclusion Intermittent fasting initiated before or after MI reduces myocyte hypertrophy and LV dilation. Myocardial fibrosis and fetal gene expression are not modulated by feeding regimens. Benefit is more evident when intermittent fasting is initiated before rather than after MI.

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N-Acetylcysteine Influence on Oxidative Stress and Cardiac Remodeling in Rats During Transition from Compensated Left Ventricular Hypertrophy to Heart Failure

Cited by 37 publications

References 48 publications

Exercise during transition from compensated left ventricular hypertrophy to heart failure in aortic stenosis rats

Exercise during transition from compensated left ventricular hypertrophy to heart failure in aortic stenosis rats

Lipoxidation in cardiovascular diseases

Influence of intermittent fasting on myocardial infarction-induced cardiac remodeling

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