Stanozolol induces ventricular dysfunction by decreasing phospholamban phosphorylation in heart tissue of LDLr-/- mice

Stanozolol is a steroid that causes lipid deposition in LDLr-/- mice, although the mechanism by which this dyslipidemia results in cardiac dysfunction is little understood. The aim of this study was to evaluate the effect of stanozolol on cardiac contractility and the participation of myocardial pho...

ver descrição completa

Detalhes bibliográficos
Autores: Andrade, Tadeu Uggere de, Dubois Fillho, Dionisio, Silva, Cristiane Lyrio da, Silva, Mirian de Almeida, Almeida, Simone Alves de, Nascimento, Andrews Marques do, Bissoli, Nazaré Souza, Brasil, Girlandia Alexandre, Lima, Ewelyne Miranda de
Formato: artículo
Estado:Versión publicada
Fecha de publicación:2022
País:Brasil
Recursos:Universidade Federal de Itajubá (UNIFEI)
Repositorio:Research, Society and Development
Idioma:inglés
OAI Identifier:oai:ojs.pkp.sfu.ca:article/27876
Acesso em linha:https://rsdjournal.org/index.php/rsd/article/view/27876
Access Level:acceso abierto
Palavra-chave:Anabolic androgenic steroids
Hemodynamic parameters
Cardiac remodeling
Phospholamban phosphorylation.
Esteróide anabolico androgênico
Parâmetros hemodinâmicos
Remodelamento cardíaco
Fosfolambam fosforilada.
Esteroide androgénico anabólico
Parámetros hemodinâmicos
Remodelado cardíaco
Fosfolambano fosforilado.
Descrição
Resumo:Stanozolol is a steroid that causes lipid deposition in LDLr-/- mice, although the mechanism by which this dyslipidemia results in cardiac dysfunction is little understood. The aim of this study was to evaluate the effect of stanozolol on cardiac contractility and the participation of myocardial phospholamban (pPLB) phosphorylation in an atherosclerosis mouse model. LDL receptor knockout mice (LDLr-/-) were fed a standard chow diet and received weekly subcutaneous injections of either saline (control, C group) or 20 mg/kg stanozolol (S group). After 8 weeks, hemodynamic parameters were assessed in the left ventricle. The heart was collected, weighted for hypertrophy evaluation, and kept in formalin buffer for morphometric analysis (H&E) and collagen quantification (Picrossirius). Protein expression of PLB and its phosphorylated form (p-PLB) in the left ventricle was determined by western blot. We observed that stanozolol treatment favored cardiac hypertrophy and collagen deposition in heart tissue. Also, stanozolol induced left ventricle dysfunction, increasing PBL expression and decreasing the p-PLB/PLB ratio. Altogether, our data showed that stanozolol causes cardiac remodeling and ventricular dysfunction by decreasing PLB phosphorylation in the left ventricle of LDLr-/- mice.