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Influence of air pollution on myocardial remodeling in experimental Chagas Disease

Grant number: 14/23941-8
Support type:Regular Research Grants
Duration: December 01, 2016 - November 30, 2018
Field of knowledge:Health Sciences - Medicine - Medical Clinics
Principal Investigator:Felix José Alvarez Ramires
Grantee:Felix José Alvarez Ramires
Home Institution: Instituto do Coração Professor Euryclides de Jesus Zerbini (INCOR). Hospital das Clínicas da Faculdade de Medicina da USP (HCFMUSP). Secretaria da Saúde (São Paulo - Estado). São Paulo , SP, Brazil
Assoc. researchers:Fernanda Gallinaro Pessoa ; Keila Cardoso Barbosa

Abstract

Chagas's disease is a major cause of cardiomyopathy and heart failure in Brazil, causing myocardial dysfunction that is characterized by fibrosis and which is directly related to a complex cascade of pathways that interrelate, such as inflammation, oxidative stress and apoptosis. As well air pollution leads to intense activation of these pathways mentioned, amplifying and intensifying the body's response against this aggression. So being in Chaga's disease which promotes the activation of a complex chain of events with intense inflammation, oxidative stress, apoptosis, and intense myocardial interstitial fibrosis; and pollution is a major factor in stimulating these same cascades of events, our hypothesis is that pollution could amplify the effects caused by these pathways stimulating oxidative stress and inflammation and leading to increased myocyte loss with consequent increasing myocardial fibrosis. 100 females Sirius Hamsters will be divided into 4 groups (CT, CT + Pollution, Infected and infected + Pollution). The animals will be exposed to pollution by inhalation of particulate matter produced after burning diesel fuel. The volume fraction of interstitial collagen in the left ventricle (ICVF-LV) and right ventricle (RV-ICVF) will be determined by histological sections stained with picrosirus red using the QWIN Image Processing and Analysis Software (Leica Microsystems Ltd Cambridge progra.). The anatomical and functional analysis will be performed by echocardiography. The evaluation of inflammation will be made by gene expression using RT-PCR in real time. Oxidative stress by ELISA and RT-PCR in real time and apoptosis by TUNEL and RT-PCR in real time also. (AU)