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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

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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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]
Total Authors: 8
[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
Total Affiliations: 4
Document type: Journal article
Source: CYTOKINE; v. 121, SEP 2019.
Web of Science Citations: 2

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)

FAPESP's process: 16/11883-9 - Role TNF-alpha on the cardiac generation of reactive oxygen species and on the reduction of nitric oxide bioavailability induced by chronic ethanol consumption
Grantee:Marcelo de Almeida Nakashima
Support type: Scholarships in Brazil - Scientific Initiation
FAPESP's process: 14/09595-0 - TNF-alpha participation in vascular dysfunction induced by chronic ethanol consumption: involvement of perivascular adipose tissue
Grantee:Janaina Aparecida Simplicio
Support type: Scholarships in Brazil - Doctorate