El estanozolol induce disfunción ventricular al reducir la fosforilación de fosfolamban en el tejido cardíaco de ratones LDLr-/-
DOI:
https://doi.org/10.33448/rsd-v11i5.27876Palabras clave:
Esteroide androgénico anabólico; Parámetros hemodinâmicos; Remodelado cardíaco; Fosfolambano fosforilado.Resumen
El estanozolol es un esteroide que promueve el depósito de lípidos en las arterias de ratones LDLr-/-, sin embargo, el mecanismo por el cual la dislipidemia promueve la disfunción cardíaca en estos animales aún no se conoce bien. Por lo tanto, el objetivo del presente estudio es evaluar el efecto del estanozolol sobre la contractilidad cardíaca y la participación de la fosforilación de la proteína fosfolambano miocárdico (pPBL) en el modelo animal de aterosclerosis. Se alimentó a ratones sin receptor de LDL (LDLr-/-) con una dieta estándar de casa de animales y recibieron inyecciones subcutáneas semanales de solución salina (grupo de control, C) o 20 mg/kg de estanozolol (grupo S). Después de ocho semanas de tratamiento, se evaluaron los parámetros hemodinámicos en el ventrículo izquierdo. Luego se recolectó el corazón, se pesó para determinar la hipertrofia y se almacenó en tampón de formalina para análisis morfométrico (H&E) y cuantificación de colágeno (picrosirius). La expresión de la proteína fosfolambano (PBL) y su forma fosforilada (p-PBL) en el ventrículo izquierdo se determinó por western blot. Observamos que el tratamiento con estanozolol favorecía la hipertrofia y el depósito de colágeno en el tejido cardíaco. Además, el estanozolol indujo disfunción ventricular izquierda, aumentó la expresión de PBL y redujo la relación p-PBL/PBL. En conjunto, nuestros datos muestran que el estanozolol promueve la remodelación cardíaca y la disfunción ventricular al reducir la fosforilación del fosfolambano del ventrículo izquierdo en ratones LDLr-/-.
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Derechos de autor 2022 Tadeu Uggere de Andrade; Dionisio Dubois Fillho; Cristiane Lyrio da Silva; Mirian de Almeida Silva; Simone Alves de Almeida; Andrews Marques do Nascimento; Nazaré Souza Bissoli; Girlandia Alexandre Brasil; Ewelyne Miranda de Lima
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