دورية أكاديمية
أعرض في EDS

Aerobic exercise prevents cardiomyocyte damage caused by oxidative stress in early cardiovascular disease by increasing vascularity while L-arginine supplementation prevents it by increasing activation of the enzyme nitric oxide synthase.

التفاصيل البيبلوغرافية
العنوان: Aerobic exercise prevents cardiomyocyte damage caused by oxidative stress in early cardiovascular disease by increasing vascularity while L-arginine supplementation prevents it by increasing activation of the enzyme nitric oxide synthase.
المؤلفون: Bertoldi JMCRJ; Departamento de Fisiologia e Farmacologia, Universidade Federal Fluminense, Niterói, Rio de Janeiro, RJ, Brasil.; Instituto Nacional de Ciência e Tecnologia - (In)atividade física e exercício, Rio de Janeiro, RJ, Brasil., Kindlovits R; Departamento de Fisiologia e Farmacologia, Universidade Federal Fluminense, Niterói, Rio de Janeiro, RJ, Brasil.; Instituto Nacional de Ciência e Tecnologia - (In)atividade física e exercício, Rio de Janeiro, RJ, Brasil., Rocha HNM; Departamento de Fisiologia e Farmacologia, Universidade Federal Fluminense, Niterói, Rio de Janeiro, RJ, Brasil.; Instituto Nacional de Ciência e Tecnologia - (In)atividade física e exercício, Rio de Janeiro, RJ, Brasil., Fernandes-Santos C; Departamento de Ciências Básicas, Universidade Federal Fluminense, Nova Friburgo, Rio de Janeiro, RJ, Brasil., Gomes JLP; Instituto Nacional de Ciência e Tecnologia - (In)atividade física e exercício, Rio de Janeiro, RJ, Brasil.; Departamento de Biodinâmica do Movimento do Corpo Humano, Universidade de São Paulo, São Paulo, SP, Brasil., Oliveira EM; Instituto Nacional de Ciência e Tecnologia - (In)atividade física e exercício, Rio de Janeiro, RJ, Brasil.; Departamento de Biodinâmica do Movimento do Corpo Humano, Universidade de São Paulo, São Paulo, SP, Brasil., Muniz IC; Departamento de Fisiologia e Farmacologia, Universidade Federal Fluminense, Niterói, Rio de Janeiro, RJ, Brasil.; Instituto Nacional de Ciência e Tecnologia - (In)atividade física e exercício, Rio de Janeiro, RJ, Brasil., Santos MM; Departamento de Fisiologia e Farmacologia, Universidade Federal Fluminense, Niterói, Rio de Janeiro, RJ, Brasil.; Instituto Nacional de Ciência e Tecnologia - (In)atividade física e exercício, Rio de Janeiro, RJ, Brasil., Pereira JF; Departamento de Fisiologia e Farmacologia, Universidade Federal Fluminense, Niterói, Rio de Janeiro, RJ, Brasil.; Instituto Nacional de Ciência e Tecnologia - (In)atividade física e exercício, Rio de Janeiro, RJ, Brasil., Rocha NG; Departamento de Fisiologia e Farmacologia, Universidade Federal Fluminense, Niterói, Rio de Janeiro, RJ, Brasil.; Instituto Nacional de Ciência e Tecnologia - (In)atividade física e exercício, Rio de Janeiro, RJ, Brasil., Nóbrega ACLD; Departamento de Fisiologia e Farmacologia, Universidade Federal Fluminense, Niterói, Rio de Janeiro, RJ, Brasil.; Instituto Nacional de Ciência e Tecnologia - (In)atividade física e exercício, Rio de Janeiro, RJ, Brasil., Medeiros RF; Instituto Nacional de Ciência e Tecnologia - (In)atividade física e exercício, Rio de Janeiro, RJ, Brasil.; Departamento de Nutrição e Dietética, Universidade Federal Fluminense, Niterói, Rio de Janeiro, RJ, Brasil.
المصدر: Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas [Braz J Med Biol Res] 2023 Aug 14; Vol. 56, pp. e12533. Date of Electronic Publication: 2023 Aug 14 (Print Publication: 2023).
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Associação Brasileira de Divulgação Científica Country of Publication: Brazil NLM ID: 8112917 Publication Model: eCollection Cited Medium: Internet ISSN: 1414-431X (Electronic) Linking ISSN: 0100879X NLM ISO Abbreviation: Braz J Med Biol Res Subsets: MEDLINE
أسماء مطبوعة: Original Publication: [SP, Brasil : Associação Brasileira de Divulgação Científica, 1981-
مواضيع طبية MeSH: Cardiovascular Diseases*/metabolism , MicroRNAs*/metabolism, Rats ; Animals ; Myocytes, Cardiac/metabolism ; Rats, Wistar ; Tumor Necrosis Factor-alpha/pharmacology ; Matrix Metalloproteinase 2/metabolism ; Nitric Oxide Synthase/metabolism ; Oxidative Stress ; Arginine/pharmacology ; Arginine/metabolism ; Insulin ; Fructose/metabolism ; Fructose/pharmacology ; Dietary Supplements ; Hypertrophy/metabolism
مستخلص: L-Arginine and chronic exercise reduce oxidative stress. However, it is unclear how they affect cardiomyocytes during cardiovascular disease (CVD) development. The aim of this research was to investigate the possible effects of L-arginine supplementation and aerobic training on systemic oxidative stress and their consequences on cardiomyocytes during cardiometabolic disease onset caused by excess fructose. Wistar rats were allocated into four groups: control (C), fructose (F, 10% fructose in water), fructose training (FT; moderate running, 50-70% of the maximal velocity), and fructose arginine (FA; 880 mg/kg/day). Fructose was given for two weeks and fructose plus treatments for the subsequent eight weeks. Body composition, blood glucose, insulin, lipid profile, lipid peroxidation, nitrite, metalloproteinase-2 (MMP-2) activity, left ventricle histological changes, microRNA-126, -195, and -146, eNOS, p-eNOS, and TNF-α expressions were analyzed. Higher abdominal fat mass, triacylglycerol level, and insulin level were observed in the F group, and both treatments reversed these alterations. Myocardial vascularization was impaired in fructose-fed groups, except in FT. Cardiomyocyte hypertrophy was observed in all fructose-fed groups. TNF-α levels were higher in fructose-fed groups than in the C group, and p-eNOS levels were higher in the FA than in the C and F groups. Lipid peroxidation was higher in the F group than in the FT and C groups. During CVD onset, moderate aerobic exercise reduced lipid peroxidation, and both training and L-arginine prevented metabolic changes caused by excessive fructose. Myocardial vascularization was impaired by fructose, and cardiomyocyte hypertrophy appeared to be influenced by pro-inflammatory and oxidative environments.
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المشرفين على المادة: 0 (Tumor Necrosis Factor-alpha)
EC 3.4.24.24 (Matrix Metalloproteinase 2)
EC 1.14.13.39 (Nitric Oxide Synthase)
94ZLA3W45F (Arginine)
0 (Insulin)
30237-26-4 (Fructose)
0 (MIRN126 microRNA, rat)
0 (MicroRNAs)
تواريخ الأحداث: Date Created: 20230816 Date Completed: 20230818 Latest Revision: 20230823
رمز التحديث: 20230823
مُعرف محوري في PubMed: PMC10427156
DOI: 10.1590/1414-431X2023e12533
PMID: 37585913
قاعدة البيانات: MEDLINE
الوصف
تدمد:1414-431X
DOI:10.1590/1414-431X2023e12533