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Evaluation of the protective action of interleukin (IL) -10 in the vascular dysfunction induced by chronic ethanol consumption

Grant number: 17/13919-3
Support Opportunities:Scholarships in Brazil - Scientific Initiation
Effective date (Start): October 01, 2017
Effective date (End): September 30, 2018
Field of knowledge:Biological Sciences - Pharmacology - Cardiorenal Pharmacology
Principal Investigator:Carlos Renato Tirapelli
Grantee:Julieth Paola Salamanca Gómez
Host Institution: Escola de Enfermagem de Ribeirão Preto (EERP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil


Chronic ethanol consumption induces significant alterations in both cardiac and circulatory functions and is considered as important risk factor in the development of cardiovascular diseases, such as hypertension. In the vasculature, ethanol consumption induces an increase in the production of reactive oxygen species (ROS) via NADPH oxidase with consequent lipoperoxidation and reduction of the bioavailability of nitric oxide (NO), an important vascular relaxing factor. In addition, ethanol consumption induces increased vascular production of pro-inflammatory cytokines such as tumor necrosis factor (TNF)-± and interleukin(IL) -6, which also participate in vascular dysfunction associated with ethanol consumption. Taken together, these responses alter the vascular function and an increased response to vasoconstrictor agents and a reduced response to vasodilatory agents is observed. IL-10 plays a vasculoprotective role by mechanisms that include a reduction in the production of ROS and pro-inflammatory cytokines (such as TNF-± and IL-6) and an increa in the endothelial production of NO. The vascular actions of IL-10 prevent the increase in blood pressure and the endothelial / vascular dysfunction observed in different experimental models. However, there are no reports describing whether IL-10 protects the vasculature from the damage caused by ethanol consumption. Considering that ethanol consumption increases blood pressure and induces vascular / endothelial dysfunction by increasing ROS production and pro-inflammatory cytokines and by reducing the bioavailability of NO, it is possible that IL-10 may modulate the cardiovascular changes induced by ethanol. The hypothesis of the present study is that IL-10 will negatively modulate the increase in blood pressure and the following vascular changes induced by ethanol consumption: production of ROS and pro-inflammatory cytokines, reduction of NO bioavailability and increase in vascular contractility. (AU)

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