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(Referência obtida automaticamente do Web of Science, por meio da informação sobre o financiamento pela FAPESP e o número do processo correspondente, incluída na publicação pelos autores.)

Chronic ethanol consumption increases reactive oxygen species generation and the synthesis of pro-inflammatory proteins in the heart through TNFR1-dependent mechanisms

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Autor(es):
Nakashima, Marcelo A. [1] ; Silva, Carla B. P. [1, 2] ; Gonzaga, Natalia A. [3, 1] ; Simplicio, Janaina A. [3, 1] ; Omoto, Ana C. M. [3] ; Tirapelli, Luis F. [3] ; Tanus-Santos, Jose E. [3] ; Tirapelli, Carlos R. [4]
Número total de Autores: 8
Afiliação do(s) autor(es):
[1] Univ Sao Paulo, DEPCH, Escola Enfermagem Ribeirao Preto, Ribeirao Preto, SP - Brazil
[2] Univ Sao Paulo, Fac Ciencias Farmaceut Ribeirao Preto, Programa Posgrad Toxicol, Ribeirao Preto, SP - Brazil
[3] Univ Sao Paulo, Fac Med Ribeirao Preto, Ribeirao Preto, SP - Brazil
[4] Univ Sao Paulo, Fac Ciencias Farmaceut Ribeirao Preto, DFQ, Escola Enfermagem Ribeirao Preto, DEPCH, Ribeirao Preto, SP - Brazil
Número total de Afiliações: 4
Tipo de documento: Artigo Científico
Fonte: CYTOKINE; v. 121, SEP 2019.
Citações Web of Science: 2
Resumo

We evaluated the role of tumor necrosis factor (TNF)-alpha receptor 1 (TNFR1) on ethanol-induced cardiac dysfunction. Male C57BL/6J wild-type (WT) or TNFR1-deficient mice (TNFR1(-/-)) were treated with ethanol (20% v/v) for 10 weeks. Increased protein expression of TNFR1 and NF kappa B p65 was detected in the left ventricle (LV) of WT mice chronically treated with ethanol. Echocardiographic analysis showed that ethanol consumption increased left ventricular posterior wall end-diastolic diameter and left ventricular posterior wall end-systolic diameter in WT, but not TNFR1(-/-) mice. Increased levels of TNF-alpha, interleukin (IL)-6, superoxide anion (O-2(center dot-)), thiobarbituric acid reactive substances (TBARS) as well as increased nitrotyrosine immunostaining were detected in the LV from WT, but not TNFR1(-/-) mice. Conversely, treatment with ethanol decreased nitrate/nitrite (NOx) concentration in the LV. Histopathological analysis showed that ethanol did not induce inflammatory infiltrates, necrosis or edema in the LV. No differences in the ventricular expression of iNOS, Nox2 or COX-2 as well as in the activity of superoxide dismutase (SOD), myeloperoxidase (MPO) and N-acetyl-beta-D-glucosaminidase (NAG) were found after treatment with ethanol. Our study provided novel evidence that ethanol consumption augmented the production of reactive oxygen species (ROS) and the synthesis of pro inflammatory proteins in the LV through TNFR1-dependent mechanisms. These findings provided novel mechanistic insights about the contribution of TNFR1 in the initial steps of the cardiac damage induced by ethanol. (AU)

Processo FAPESP: 16/11883-9 - Participação do TNF-alfa na geração cardíaca de espécies reativas de oxigênio e na redução da biodisponibilidade de óxido nítrico induzida pelo consumo crônico de etanol
Beneficiário:Marcelo de Almeida Nakashima
Linha de fomento: Bolsas no Brasil - Iniciação Científica
Processo FAPESP: 14/09595-0 - Participação do TNF-alfa nas disfunções vasculares induzidas pelo consumo crônico de etanol: envolvimento do tecido adiposo perivascular
Beneficiário:Janaina Aparecida Simplicio
Linha de fomento: Bolsas no Brasil - Doutorado