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  2. Keyword: NADPH Oxidase
Figure 1
ABC
Original Article

Effects of Late Aerobic Exercise on Cardiac Remodeling of Rats with Small-Sized Myocardial Infarction

Lidiane M. Souza et al. Marina P. Okoshi Mariana J. Gomes Mariana Gatto … Eder A. Rodrigues Thierres H. D. Pontes Felipe C. Damatto Leiliane R. S. Oliveira Patrícia Aparecida Borim Aline R. R. Lima Leonardo A. M. Zornoff Katashi Okoshi Luana U. Pagan

Abstract

Background:

Physical exercise has been considered an important non-pharmacological therapy for the prevention and treatment of cardiovascular diseases. However, its effects on minor cardiac remodeling are not clear.

Objective:

To evaluate the influence of aerobic exercise on the functional capacity, cardiac structure, left ventricular (LV) function, and gene expression of NADPH oxidase subunits in rats with small-sized myocardial infarction (MI).

Methods:

Three months after MI induction, Wistar rats were divided into three groups: Sham; sedentary MI (MI-SED); and aerobic exercised MI (MI-AE). The rats exercised on a treadmill three times a week for 12 weeks. An echocardiogram was performed before and after training. The infarction size was evaluated by histology, and gene expression was assessed by RT-PCR. The significance level for statistical analysis was set at 5%.

Results:

Rats with MI lower than 30% of the LV total area were included in the study. Functional capacity was higher in MI-AE than in Sham and MI-SED rats. The infarction size did not differ between groups. Infarcted rats had increased LV diastolic and systolic diameter, left atrial diameter, and LV mass, with systolic dysfunction. Relative wall thickness was lower in MI-SED than in the MI-AE and Sham groups. Gene expression of the NADPH oxidase subunits NOX2, NOX4, p22phox, and p47phox did not differ between groups.

Conclusion:

Small-sized MI changes cardiac structure and LV systolic function. Late aerobic exercise is able to improve functional capacity and cardiac remodeling by preserving the left ventricular geometry. NADPH oxidase subunits gene expression is not involved in cardiac remodeling or modulated by aerobic exercise in rats with small-sized MI.

  • Echocardiography/methods
  • Exercise, Physical Exercise
  • Myocardial Infarction
  • NADPH Oxidase
  • Rats
  • Ventricular Dysfunction
  • Ventricular Remodeling
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Creative Commons Attribution (CC BY) Creative Commons license
16/04/2021 DOI: 10.36660/abc.20190813 Views 1
Figure 1
ABC
Original Article

Acute Ethanol Intake Induces NAD(P)H Oxidase Activation and Rhoa Translocation in Resistance Arteries

Janaina A. Simplicio et al. Ulisses Vilela Hipólito Gabriel Tavares do Vale Glaucia Elena Callera … Camila André Pereira Rhian M Touyz Rita de Cássia Tostes Carlos R. Tirapelli

Abstract

Background:

The mechanism underlying the vascular dysfunction induced by ethanol is not totally understood. Identification of biochemical/molecular mechanisms that could explain such effects is warranted.

Objective:

To investigate whether acute ethanol intake activates the vascular RhoA/Rho kinase pathway in resistance arteries and the role of NAD(P)H oxidase-derived reactive oxygen species (ROS) on such response. We also evaluated the requirement of p47phox translocation for ethanol-induced NAD(P)H oxidase activation.

Methods:

Male Wistar rats were orally treated with ethanol (1g/kg, p.o. gavage) or water (control). Some rats were treated with vitamin C (250 mg/kg, p.o. gavage, 5 days) before administration of water or ethanol. The mesenteric arterial bed (MAB) was collected 30 min after ethanol administration.

Results:

Vitamin C prevented ethanol-induced increase in superoxide anion (O2–) generation and lipoperoxidation in the MAB. Catalase and superoxide dismutase activities and the reduced glutathione, nitrate and hydrogen peroxide (H2O2) levels were not affected by ethanol. Vitamin C and 4-methylpyrazole prevented the increase on O2– generation induced by ethanol in cultured MAB vascular smooth muscle cells. Ethanol had no effect on phosphorylation levels of protein kinase B (Akt) and eNOS (Ser1177 or Thr495 residues) or MAB vascular reactivity. Vitamin C prevented ethanol-induced increase in the membrane: cytosol fraction ratio of p47phox and RhoA expression in the rat MAB.

Conclusion:

Acute ethanol intake induces activation of the RhoA/Rho kinase pathway by a mechanism that involves ROS generation. In resistance arteries, ethanol activates NAD(P)H oxidase by inducing p47phox translocation by a redox-sensitive mechanism.

  • Ascorbic acid
  • Ethanol
  • NADPH Oxidase
  • Oxidative Stress
  • Rats
  • rhoAGTP-Binding Protein
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Creative Commons Attribution (CC BY) Creative Commons license
27/10/2016 DOI: 10.5935/abc.20160147 Views 1
Redox unbalance: NADPH oxidase as therapeutic target in blood pressure control
ABC
Review Article

Redox unbalance: NADPH oxidase as therapeutic target in blood pressure control

Luiza A. Rabêlo et al. Valéria Nunes de Souza Lucas José Sá da Fonseca Walkyria O. Sampaio

Several studies refer to reactive oxygen and nitrogen species (RONS) as important agents in the pathogenesis of a number of heart diseases, including high blood pressure, arteriosclerosis and heart failure. Such species are highly bioactive molecules and a short life due chiefly to reduction of molecular oxygen. The enzyme complex of NADPH oxidase is the main source of these reactive species in vascular system. Under physiological conditions, formation and elimination of these substances seem balanced in vascular wall. During redox Unbalance, nonetheless, there is increase in NADPH oxidase activity and predominance of pro-oxidizing agents, surpassing the anti-oxidant capacity of the organism self-defense. Besides this, such enzyme hyperactivity reduces the bioavailability of nitric oxide, capital for vasodilation and maintenance of normal vascular function. In spite of NADPH oxidase being directly connected to the endothelial dysfunction, it was firstly described as for its expression in phagocytes, where its activity determines efficiency of organism defense mechanisms against pathogens. Slight differences between structural units of NADPH oxidases, depending on the type of cell which expresses it, may create therapeutic implications, allowing to selectively inhibiting redox unbalance triggered by NADPH oxidase, without compromising, however, its participation in physiological cellular signaling which make sure protection against micro-organisms.

  • Cardiovascular Diseases
  • NADPH Oxidase
  • NADPH oxidase inhibitors
  • Oxidation-Reduction
  • reactive nitrogen species
  • Reactive Oxygen Species
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Creative Commons Attribution (CC BY) Creative Commons license
22/09/2010 DOI: 10.1590/S0066-782X2010000500018

How to cite this article

EndNote RIS

Electronic Document Format (Vancouver)

Souza LM, Okoshi MP, Gomes MJ, Gatto M, Rodrigues EA, Pontes THD, Damatto FC, et al. Effects of Late Aerobic Exercise on Cardiac Remodeling of Rats with Small-Sized Myocardial Infarction. Arquivos Brasileiros de Cardiologia 2021;116(4):784-92.

Electronic Document Format (ABNT)

Souza, Lidiane M.; Okoshi, Marina P.; Gomes, Mariana J.; Gatto, Mariana; Rodrigues, Eder A.; Pontes, Thierres H. D.; Damatto, Felipe C.; Oliveira, Leiliane R. S.; Borim, Patrícia Aparecida; Lima, Aline R. R.; Zornoff, Leonardo A. M.; Okoshi, Katashi; Pagan, Luana U.. Effects of Late Aerobic Exercise on Cardiac Remodeling of Rats with Small-Sized Myocardial Infarction. Arquivos Brasileiros de Cardiologia, v. 116, n. 4, p. 784-792, Apr. 2021.

Electronic Document Format (APA)

Souza, L. M., Okoshi, M. P., Gomes, M. J., Gatto, M., Rodrigues, E. A., Pontes, T. H. D., Damatto, F. C., Oliveira, L. R. S., Borim, P. A., Lima, A. R. R., Zornoff, L. A. M., Okoshi, K., & Pagan, L. U. (2021). Effects of Late Aerobic Exercise on Cardiac Remodeling of Rats with Small-Sized Myocardial Infarction. Arquivos Brasileiros de Cardiologia, 116(4), 784-792.

Electronic Document Format (ISO)

Souza, Lidiane M. and Okoshi, Marina P. and Gomes, Mariana J. and Gatto, Mariana and Rodrigues, Eder A. and Pontes, Thierres H. D. and Damatto, Felipe C. and Oliveira, Leiliane R. S. and Borim, Patrícia Aparecida and Lima, Aline R. R. and Zornoff, Leonardo A. M. and Okoshi, Katashi and Pagan, Luana U.. Effects of Late Aerobic Exercise on Cardiac Remodeling of Rats with Small-Sized Myocardial Infarction. Arquivos Brasileiros de Cardiologia [online]. 2021, vol. 116, n. 4, [cited 2026-10-14], pp. 784-792. Available from: <https://journals.cardiol.br/en/article/effects-of-late-aerobic-exercise-on-cardiac-remodeling-of-rats-with-small-sized-myocardial-infarction/>. ISSN 0066-782X

EndNote RIS

Electronic Document Format (Vancouver)

Simplicio JA, Hipólito UV, Vale GT, Callera GE, Pereira CA, Touyz RM, Tostes RC, et al. Acute Ethanol Intake Induces NAD(P)H Oxidase Activation and Rhoa Translocation in Resistance Arteries. Arquivos Brasileiros de Cardiologia 2016;107(5):427-36.

Electronic Document Format (ABNT)

Simplicio, Janaina A.; Hipólito, Ulisses Vilela; Vale, Gabriel Tavares do; Callera, Glaucia Elena; Pereira, Camila André; Touyz, Rhian M; Tostes, Rita de Cássia; Tirapelli, Carlos R.. Acute Ethanol Intake Induces NAD(P)H Oxidase Activation and Rhoa Translocation in Resistance Arteries. Arquivos Brasileiros de Cardiologia, v. 107, n. 5, p. 427-436, Oct. 2016.

Electronic Document Format (APA)

Simplicio, J. A., Hipólito, U. V., Vale, G. T. , Callera, G. E., Pereira, C. A., Touyz, R. M., Tostes, R. C., & Tirapelli, C. R. (2016). Acute Ethanol Intake Induces NAD(P)H Oxidase Activation and Rhoa Translocation in Resistance Arteries. Arquivos Brasileiros de Cardiologia, 107(5), 427-436.

Electronic Document Format (ISO)

Simplicio, Janaina A. and Hipólito, Ulisses Vilela and Vale, Gabriel Tavares do and Callera, Glaucia Elena and Pereira, Camila André and Touyz, Rhian M and Tostes, Rita de Cássia and Tirapelli, Carlos R.. Acute Ethanol Intake Induces NAD(P)H Oxidase Activation and Rhoa Translocation in Resistance Arteries. Arquivos Brasileiros de Cardiologia [online]. 2016, vol. 107, n. 5, [cited 2026-10-14], pp. 427-436. Available from: <https://journals.cardiol.br/en/article/acute-ethanol-intake-induces-nadph-oxidase-activation-and-rhoa-translocation-in-resistance-arteries/>. ISSN 0066-782X

EndNote RIS

Electronic Document Format (Vancouver)

Rabêlo LA, Souza VN, Fonseca LJS, Sampaio WO. Redox unbalance: NADPH oxidase as therapeutic target in blood pressure control. Arquivos Brasileiros de Cardiologia 2010;94(5):684-93.

Electronic Document Format (ABNT)

Rabêlo, Luiza A.; Souza, Valéria Nunes de; Fonseca, Lucas José Sá da; Sampaio, Walkyria O.. Redox unbalance: NADPH oxidase as therapeutic target in blood pressure control. Arquivos Brasileiros de Cardiologia, v. 94, n. 5, p. 684-693, Sep. 2010.

Electronic Document Format (APA)

Rabêlo, L. A., Souza, V. N. , Fonseca, L. J. S. , & Sampaio, W. O. (2010). Redox unbalance: NADPH oxidase as therapeutic target in blood pressure control. Arquivos Brasileiros de Cardiologia, 94(5), 684-693.

Electronic Document Format (ISO)

Rabêlo, Luiza A. and Souza, Valéria Nunes de and Fonseca, Lucas José Sá da and Sampaio, Walkyria O.. Redox unbalance: NADPH oxidase as therapeutic target in blood pressure control. Arquivos Brasileiros de Cardiologia [online]. 2010, vol. 94, n. 5, [cited 2026-10-14], pp. 684-693. Available from: <https://journals.cardiol.br/en/article/redox-unbalance-nadph-oxidase-as-therapeutic-target-in-blood-pressure-control/>. ISSN 0066-782X

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