Angiotensin-(1-7) oral treatment after experimental myocardial infarction leads to downregulation of CXCR4
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Universidade Federal de Minas Gerais
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Artigo de periódico
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Membros da banca
Resumo
Myocardial infarction triggers cellular events that starts with the activation of inflammatory response and fibrogenic pathways involved in cardiac tissue remodeling. Angiotensin-(1–7) (Ang-(1–7)) is an endogenous heptapeptide from the renin-angiotensin system with a cardioprotective role due to its anti-inflammatory and anti-fibrotic activities in cardiac cells. Although the beneficial aspects of Ang-(1–7) in animal models of cardiac ischemia have been reported, the molecular events underlying Ang-(1–7) cardioprotective effect remains elusive. This study investigated the impact of oral treatment with Ang-(1–7) included in hydroxypropyl β-cyclodextrin (HPβCD/Ang-(1–7)) on the cardiac proteome dysregulation due to experimental myocardial infarction. Wistar male rats were submitted to experimental myocardial infarction and treated daily with HPβCD/Ang-(1–7) during 7 days or 60 days by gavage. Our results showed that HPβCD/Ang-(1–7) treatment ameliorates the post-infarction condition due to the modulation of proteins that initially favor the resolution of inflammation and mitochondrial dysfunction. Moreover, this study reported for the first time that Ang-(1–7) treatment after experimental myocardial infarction leads to the downregulation of the C-X-C chemokine receptor type 4 (CXCR4).
Abstract
Assunto
Angiotensina, Enfarte do miocárdio, Agentes antiinflamatórios, Ciclodextrinas
Palavras-chave
Angiotensin-(1–7), Anti-inflammatory, Myocardial infarction, Proteomics, CXCR4
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https://www.sciencedirect.com/science/article/pii/S1874391919302581