Aortic morphological changes in Metabolic Syndrome: Therapeutic contrast with atorvastatin and sleeve gastrectomy

The atherosclerotic pathogenesis of Metabolic Syndrome (MS) comes from oxidative stress (OS) and systemic endothelial inflammation. Reactive oxygen species (ROS) damage membrane proteins, DNA, and lipids, resulting in mitochondrial dysfunction and increased ROS production, causing a vicious circle t...

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Autores principales: Rossi, MM, Castillo, TA, Müller Gudiño, SE, Lescano, LA, Fonseca, L, Scribano Parada , MP, Baez, MC
Formato: Artículo revista
Publicado: Universidad Nacional Córdoba. Facultad de Ciencias Médicas. Secretaria de Ciencia y Tecnología 2022
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Acceso en línea:https://revistas.unc.edu.ar/index.php/med/article/view/38979
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record_format ojs
institution Universidad Nacional de Córdoba
institution_str I-10
repository_str R-327
container_title_str Revista de la Facultad de Ciencias Médicas de Córdoba
format Artículo revista
topic síndrome metabólico
estrés oxidativo
atorvastatina
gastrectomía en manga
mitocondria
spellingShingle síndrome metabólico
estrés oxidativo
atorvastatina
gastrectomía en manga
mitocondria
Rossi, MM
Castillo, TA
Müller Gudiño, SE
Lescano, LA
Fonseca, L
Scribano Parada , MP
Baez, MC
Aortic morphological changes in Metabolic Syndrome: Therapeutic contrast with atorvastatin and sleeve gastrectomy
topic_facet síndrome metabólico
estrés oxidativo
atorvastatina
gastrectomía en manga
mitocondria
author Rossi, MM
Castillo, TA
Müller Gudiño, SE
Lescano, LA
Fonseca, L
Scribano Parada , MP
Baez, MC
author_facet Rossi, MM
Castillo, TA
Müller Gudiño, SE
Lescano, LA
Fonseca, L
Scribano Parada , MP
Baez, MC
author_sort Rossi, MM
title Aortic morphological changes in Metabolic Syndrome: Therapeutic contrast with atorvastatin and sleeve gastrectomy
title_short Aortic morphological changes in Metabolic Syndrome: Therapeutic contrast with atorvastatin and sleeve gastrectomy
title_full Aortic morphological changes in Metabolic Syndrome: Therapeutic contrast with atorvastatin and sleeve gastrectomy
title_fullStr Aortic morphological changes in Metabolic Syndrome: Therapeutic contrast with atorvastatin and sleeve gastrectomy
title_full_unstemmed Aortic morphological changes in Metabolic Syndrome: Therapeutic contrast with atorvastatin and sleeve gastrectomy
title_sort aortic morphological changes in metabolic syndrome: therapeutic contrast with atorvastatin and sleeve gastrectomy
description The atherosclerotic pathogenesis of Metabolic Syndrome (MS) comes from oxidative stress (OS) and systemic endothelial inflammation. Reactive oxygen species (ROS) damage membrane proteins, DNA, and lipids, resulting in mitochondrial dysfunction and increased ROS production, causing a vicious circle that keeps an inflammatory state and OS in the aortic wall. Pharmacological treatment with atorvastatin and surgical intervention by sleeve gastrectomy (SG) are therapies used to reduce the rate of cardiovascular events in MS. The purpose of the present study was to analyze and compare the aortic morphological changes after treatment with atorvastatin and SG in an experimental model of MS. We used 32 male rats (Wistar) divided into the following groups: Control (C)(n=8), SM(n=8), MS+atorvastatin(MS+A)(n=8) and MS+SG(MS+SG)(n =8). SM was induced by administering 10% fructose in drinking water for 60 days. Atorvastatin 10 mg was used for 45 days. SG was performed achieving a 80% of gastric restriction. Histological sections of the thoracic aorta were analyzed by light microscopy (MO) and electron microscopy (ME). The control group showed undamaged endothelium and elastic aortic walls preserved. In MS group, we observed sectors of endothelial denudation and myxoid areas. The MS+SG group showed thickened vessel walls and myxoid areas, without significant changes. The OM of MS+A showed regression of the lesion at the endothelial level. Mitocondrial size and shape were normal in the control group. In MS groups, we identified notable mitochondrial changes in the aortic muscularis with loss of electron density of the mitochondrial matrix and cristae disorganization. The MS+SG group showed a greater endothelial damage with vesicularization of the cytoplasm and changes in smooth muscle cells, also presenting irregular cell limits. Finally, in the MS+A group we observed a decreased swelling with reorganization of the matrix and cristae. Endothelial dysfunction in MS is a consequence of mitochondrial changes that lead to damage in endothelium features. Pharmacological treatment with atorvastatin could reduce cardiovascular risk in MS by improving vascular damage by reversing mitochondrial alterations. However, these benefits have not been seen with surgical treatment. The study of aortic histological changes and mitochondrial architecture may lead to new treatment strategies for MS and the risk of cardiovascular events.
publisher Universidad Nacional Córdoba. Facultad de Ciencias Médicas. Secretaria de Ciencia y Tecnología
publishDate 2022
url https://revistas.unc.edu.ar/index.php/med/article/view/38979
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spelling I10-R327-article-389792024-04-15T16:14:45Z Aortic morphological changes in Metabolic Syndrome: Therapeutic contrast with atorvastatin and sleeve gastrectomy Cambios morfológicos aórticos en Síndrome Metabólico: Contraste terapéutico con atorvastatina y gastrectomía en manga Rossi, MM Castillo, TA Müller Gudiño, SE Lescano, LA Fonseca, L Scribano Parada , MP Baez, MC síndrome metabólico estrés oxidativo atorvastatina gastrectomía en manga mitocondria The atherosclerotic pathogenesis of Metabolic Syndrome (MS) comes from oxidative stress (OS) and systemic endothelial inflammation. Reactive oxygen species (ROS) damage membrane proteins, DNA, and lipids, resulting in mitochondrial dysfunction and increased ROS production, causing a vicious circle that keeps an inflammatory state and OS in the aortic wall. Pharmacological treatment with atorvastatin and surgical intervention by sleeve gastrectomy (SG) are therapies used to reduce the rate of cardiovascular events in MS. The purpose of the present study was to analyze and compare the aortic morphological changes after treatment with atorvastatin and SG in an experimental model of MS. We used 32 male rats (Wistar) divided into the following groups: Control (C)(n=8), SM(n=8), MS+atorvastatin(MS+A)(n=8) and MS+SG(MS+SG)(n =8). SM was induced by administering 10% fructose in drinking water for 60 days. Atorvastatin 10 mg was used for 45 days. SG was performed achieving a 80% of gastric restriction. Histological sections of the thoracic aorta were analyzed by light microscopy (MO) and electron microscopy (ME). The control group showed undamaged endothelium and elastic aortic walls preserved. In MS group, we observed sectors of endothelial denudation and myxoid areas. The MS+SG group showed thickened vessel walls and myxoid areas, without significant changes. The OM of MS+A showed regression of the lesion at the endothelial level. Mitocondrial size and shape were normal in the control group. In MS groups, we identified notable mitochondrial changes in the aortic muscularis with loss of electron density of the mitochondrial matrix and cristae disorganization. The MS+SG group showed a greater endothelial damage with vesicularization of the cytoplasm and changes in smooth muscle cells, also presenting irregular cell limits. Finally, in the MS+A group we observed a decreased swelling with reorganization of the matrix and cristae. Endothelial dysfunction in MS is a consequence of mitochondrial changes that lead to damage in endothelium features. Pharmacological treatment with atorvastatin could reduce cardiovascular risk in MS by improving vascular damage by reversing mitochondrial alterations. However, these benefits have not been seen with surgical treatment. The study of aortic histological changes and mitochondrial architecture may lead to new treatment strategies for MS and the risk of cardiovascular events. La patogenia aterosclerótica del Síndrome Metabólico(SM) procede del estrés oxidativo(EO) y la inflamación sistémica endotelial. Las especies reactivas de oxígeno(ROS) dañan proteínas, ADN y lípidos de membranas induciendo disfunción mitocondrial y mayor producción de ROS, generando un círculo vicioso que sustenta un estado inflamatorio y EO en la pared aórtica. El tratamiento farmacológico con atorvastatina y la intervención quirúrgica mediante gastrectomía en manga(GM) son  terapéuticas utilizadas para disminuir las tasas de eventos cardiovasculares en SM. El objetivo del presente trabajo fue analizar y comparar los cambios morfológicos aórticos posteriores al tratamiento con atorvastatina y GM en un modelo experimental de SM. Utilizamos 32 ratas macho(Wistar) divididas: Control (C)(n=8), SM(n=8), SM+atorvastatina(SM+A)(n=8) y SM+GM(SM+GM)(n=8). SM se indujo administrando fructosa al 10% en agua bebida durante 60 días. Se utilizó 10 mg de atorvastatina durante 45 días. Se realizó GM asegurando una restricción gástrica del 80%. Se analizaron cortes histológicos de aorta torácica por microscopía óptica(MO) y microscopía electrónica(ME). El grupo control evidenció endotelio indemne y pared elásticas conservadas. En SM se observaron sectores de denudación endotelial y áreas mixoide. El grupo SM+GM mostró vasos de paredes engrosadas y áreas mixoides, sin cambios significativos. La MO de SM+A, demostró regresión de la lesión a nivel endotelial. La ME mitocondrial del grupo control expuso, mitocondrias de forma y tamaño normal. En SM se identificaron marcados cambios mitocondriales en la túnica muscular aórtica con pérdida de la electrodensidad de la matriz mitocondrial y desorganización de crestas. El grupo SM+GM revelo un mayor daño endotelial con vesicularización del citoplasma y cambios en células musculares lisas, presentando además límites celulares irregulares. Por último, el grupo SM+A expuso una disminución de la tumefacción con reorganización de la matriz y de las crestas. SM genera lesiones a nivel endotelial al producir cambios mitocondriales que derivan en disfunción del endotelio. El tratamiento farmacológico con atorvastatina podría disminuir el riesgo cardiovascular en SM al mejorar el daño vascular revirtiendo las alteraciones mitocondriales. Sin embargo, estos beneficios no se han observado con el tratamiento quirúrgico. El estudio de cambios histológicos aórticos y la arquitectura mitocondrial puede conducir a nuevas estrategias de tratamiento para SM y el riesgo de eventos cardiovasculares. Universidad Nacional Córdoba. Facultad de Ciencias Médicas. Secretaria de Ciencia y Tecnología 2022-10-26 info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion texto https://revistas.unc.edu.ar/index.php/med/article/view/38979 Revista de la Facultad de Ciencias Médicas de Córdoba.; Vol. 79 No. Suplemento JIC XXIII (2022): Suplemento JIC XXIII Revista de la Facultad de Ciencias Médicas de Córdoba; Vol. 79 Núm. Suplemento JIC XXIII (2022): Suplemento JIC XXIII Revista da Faculdade de Ciências Médicas de Córdoba; v. 79 n. Suplemento JIC XXIII (2022): Suplemento JIC XXIII 1853-0605 0014-6722 Derechos de autor 2022 Universidad Nacional de Córdoba http://creativecommons.org/licenses/by-nc/4.0