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

Chronic ethanol consumption increases reactive oxygen species generation and the synthesis of pro-inflammatory proteins in the heart through TNFR1-dependent mechanisms. Cytokine. 2019 May 28;121:154734 Authors: Nakashima MA, Silva CBP, Gonzaga NA, Simplicio JA, Omoto ACM, Tirapelli LF, Tanus-Santos JE, Tirapelli CR Abstract We evaluated the role of tumor necrosis factor (TNF)-α 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 NFκB 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-α, interleukin (IL)-6, superoxide anion (O2-), 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 dismuta...
Source: Cytokine - Category: Molecular Biology Authors: Tags: Cytokine Source Type: research