Efectos de Aloe-emodina en la aterosclerosis temprana inducida en modelo de larva de pez cebra alimentada con dieta alta en colesterol.
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Date
2026
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Universidad de Concepción
Abstract
La aterosclerosis es una enfermedad inflamatoria crónica caracterizada por la acumulación progresiva de lípidos y células inmunitarias en la pared arterial, lo que conduce a la formación de placas ateromatosas capaces de comprometer el flujo sanguíneo y generar eventos cardiovasculares mayores. Debido a su desarrollo lento y generalmente asintomático en etapas tempranas, comprender los mecanismos iniciales de la aterogénesis continúa siendo un desafío. En este contexto, el pez cebra (Danio rerio) ha emergido como un modelo vertebrado relevante para el estudio de enfermedades cardiovasculares, ya que comparte características del metabolismo lipídico con los humanos y permite la observación directa de procesos celulares y vasculares in vivo durante el desarrollo temprano.
La aloe-emodina (AE) es una antraquinona presente en diversas especies vegetales, como Aloe vera, Rheum palmatum y Cassia occidentalis, que ha demostrado propiedades antiinflamatorias, antioxidantes y moduladoras del metabolismo lipídico. El objetivo de este estudio fue evaluar el efecto de la aloe-emodina sobre la acumulación de células inflamatorias y depósitos lipídicos en un modelo de aterosclerosis temprana inducido por dieta alta en colesterol en larvas de pez cebra.
Inicialmente se determinaron concentraciones sub-tóxicas de AE mediante ensayos de toxicidad aguda, estableciendo concentraciones inferiores a 3 μM como seguras para su uso experimental. Posteriormente, las larvas fueron alimentadas durante 10 días con una dieta suplementada con 4% de colesterol y tratadas con AE mediante inmersión diaria. Se evaluaron parámetros de supervivencia, crecimiento larvario, marcadores bioquímicos asociados al metabolismo lipídico e inflamación, cuantificación de granulocitos mediante tinción con Sudan Black B y acumulación de depósitos lipídicos hepáticos y vasculares mediante tinciones histológicas.
Los resultados mostraron que la dieta suplementada con colesterol indujo alteraciones compatibles con un estado proaterogénico temprano, incluyendo incremento de granulocitos en la región vascular, aumento de depósitos lipídicos hepáticos y vasculares, modificaciones morfométricas del sistema vascular y tendencias al aumento de marcadores bioquímicos asociados a inflamación y metabolismo lipídico. En contraste, el tratamiento con aloe-emodina redujo significativamente la infiltración de granulocitos y la acumulación de lípidos, además de atenuar las alteraciones bioquímicas inducidas por la dieta hipercolesterolémica.
En conjunto, estos resultados sugieren que la aloe-emodina ejerce un efecto modulador sobre procesos inflamatorios y metabólicos asociados a la aterogénesis temprana, evidenciando su potencial como compuesto bioactivo en estrategias preventivas dirigidas a enfermedades cardiovasculares.
Atherosclerosis is a chronic inflammatory disease characterized by the progressive accumulation of lipids and immune cells within the arterial wall, leading to the formation of atherosclerotic plaques that can impair blood flow and trigger major cardiovascular events. Because this disease develops slowly and often remains asymptomatic during its early stages, understanding the mechanisms involved in early atherogenesis remains a major challenge. In this context, the zebrafish (Danio rerio) has emerged as a valuable vertebrate model for cardiovascular research due to similarities in lipid metabolism with humans and the possibility of directly visualizing cellular and vascular processes in vivo during early development. Aloe-emodin (AE) is an anthraquinone compound present in several plant species, including Aloe vera, Rheum palmatum, and Cassia occidentalis. This compound has demonstrated multiple pharmacological properties, such as anti-inflammatory, antioxidant, and lipid-regulating effects. The aim of this study was to evaluate the effect of aloe-emodin on inflammatory cell accumulation and lipid deposition in a zebrafish larval model of early atherosclerosis induced by a high-cholesterol diet. Initially, sub-toxic concentrations of AE were determined through acute toxicity assays, establishing concentrations below 3 μM as safe for experimental use. Zebrafish larvae were then fed for 10 days with a diet supplemented with 4% cholesterol and treated daily with AE by immersion. Several parameters were evaluated, including larval survival, growth, biochemical markers associated with lipid metabolism and inflammation, granulocyte quantification using Sudan Black B staining, and hepatic and vascular lipid deposition using histological staining techniques. The results showed that the cholesterol-enriched diet induced alterations consistent with an early pro-atherogenic state, including increased granulocyte accumulation in the vascular region, enhanced hepatic and vascular lipid deposition, vascular morphometric changes, and trends toward elevated biochemical markers related to inflammation and lipid metabolism. In contrast, treatment with aloe-emodin significantly reduced granulocyte infiltration and lipid deposition, while attenuating several biochemical alterations induced by the hypercholesterolemic diet. Overall, these findings suggest that aloe-emodin modulates inflammatory and metabolic processes involved in early atherogenesis, highlighting its potential as a bioactive compound for preventive strategies against cardiovascular diseases.
Atherosclerosis is a chronic inflammatory disease characterized by the progressive accumulation of lipids and immune cells within the arterial wall, leading to the formation of atherosclerotic plaques that can impair blood flow and trigger major cardiovascular events. Because this disease develops slowly and often remains asymptomatic during its early stages, understanding the mechanisms involved in early atherogenesis remains a major challenge. In this context, the zebrafish (Danio rerio) has emerged as a valuable vertebrate model for cardiovascular research due to similarities in lipid metabolism with humans and the possibility of directly visualizing cellular and vascular processes in vivo during early development. Aloe-emodin (AE) is an anthraquinone compound present in several plant species, including Aloe vera, Rheum palmatum, and Cassia occidentalis. This compound has demonstrated multiple pharmacological properties, such as anti-inflammatory, antioxidant, and lipid-regulating effects. The aim of this study was to evaluate the effect of aloe-emodin on inflammatory cell accumulation and lipid deposition in a zebrafish larval model of early atherosclerosis induced by a high-cholesterol diet. Initially, sub-toxic concentrations of AE were determined through acute toxicity assays, establishing concentrations below 3 μM as safe for experimental use. Zebrafish larvae were then fed for 10 days with a diet supplemented with 4% cholesterol and treated daily with AE by immersion. Several parameters were evaluated, including larval survival, growth, biochemical markers associated with lipid metabolism and inflammation, granulocyte quantification using Sudan Black B staining, and hepatic and vascular lipid deposition using histological staining techniques. The results showed that the cholesterol-enriched diet induced alterations consistent with an early pro-atherogenic state, including increased granulocyte accumulation in the vascular region, enhanced hepatic and vascular lipid deposition, vascular morphometric changes, and trends toward elevated biochemical markers related to inflammation and lipid metabolism. In contrast, treatment with aloe-emodin significantly reduced granulocyte infiltration and lipid deposition, while attenuating several biochemical alterations induced by the hypercholesterolemic diet. Overall, these findings suggest that aloe-emodin modulates inflammatory and metabolic processes involved in early atherogenesis, highlighting its potential as a bioactive compound for preventive strategies against cardiovascular diseases.
Atherosclerosis is a chronic inflammatory disease characterized by the progressive accumulation of lipids and immune cells within the arterial wall, leading to the formation of atherosclerotic plaques that can impair blood flow and trigger major cardiovascular events. Because this disease develops slowly and often remains asymptomatic during its early stages, understanding the mechanisms involved in early atherogenesis remains a major challenge. In this context, the zebrafish (Danio rerio) has emerged as a valuable vertebrate model for cardiovascular research due to similarities in lipid metabolism with humans and the possibility of directly visualizing cellular and vascular processes in vivo during early development. Aloe-emodin (AE) is an anthraquinone compound present in several plant species, including Aloe vera, Rheum palmatum, and Cassia occidentalis. This compound has demonstrated multiple pharmacological properties, such as anti-inflammatory, antioxidant, and lipid-regulating effects. The aim of this study was to evaluate the effect of aloe-emodin on inflammatory cell accumulation and lipid deposition in a zebrafish larval model of early atherosclerosis induced by a high-cholesterol diet. Initially, sub-toxic concentrations of AE were determined through acute toxicity assays, establishing concentrations below 3 μM as safe for experimental use. Zebrafish larvae were then fed for 10 days with a diet supplemented with 4% cholesterol and treated daily with AE by immersion. Several parameters were evaluated, including larval survival, growth, biochemical markers associated with lipid metabolism and inflammation, granulocyte quantification using Sudan Black B staining, and hepatic and vascular lipid deposition using histological staining techniques. The results showed that the cholesterol-enriched diet induced alterations consistent with an early pro-atherogenic state, including increased granulocyte accumulation in the vascular region, enhanced hepatic and vascular lipid deposition, vascular morphometric changes, and trends toward elevated biochemical markers related to inflammation and lipid metabolism. In contrast, treatment with aloe-emodin significantly reduced granulocyte infiltration and lipid deposition, while attenuating several biochemical alterations induced by the hypercholesterolemic diet. Overall, these findings suggest that aloe-emodin modulates inflammatory and metabolic processes involved in early atherogenesis, highlighting its potential as a bioactive compound for preventive strategies against cardiovascular diseases.
Atherosclerosis is a chronic inflammatory disease characterized by the progressive accumulation of lipids and immune cells within the arterial wall, leading to the formation of atherosclerotic plaques that can impair blood flow and trigger major cardiovascular events. Because this disease develops slowly and often remains asymptomatic during its early stages, understanding the mechanisms involved in early atherogenesis remains a major challenge. In this context, the zebrafish (Danio rerio) has emerged as a valuable vertebrate model for cardiovascular research due to similarities in lipid metabolism with humans and the possibility of directly visualizing cellular and vascular processes in vivo during early development. Aloe-emodin (AE) is an anthraquinone compound present in several plant species, including Aloe vera, Rheum palmatum, and Cassia occidentalis. This compound has demonstrated multiple pharmacological properties, such as anti-inflammatory, antioxidant, and lipid-regulating effects. The aim of this study was to evaluate the effect of aloe-emodin on inflammatory cell accumulation and lipid deposition in a zebrafish larval model of early atherosclerosis induced by a high-cholesterol diet. Initially, sub-toxic concentrations of AE were determined through acute toxicity assays, establishing concentrations below 3 μM as safe for experimental use. Zebrafish larvae were then fed for 10 days with a diet supplemented with 4% cholesterol and treated daily with AE by immersion. Several parameters were evaluated, including larval survival, growth, biochemical markers associated with lipid metabolism and inflammation, granulocyte quantification using Sudan Black B staining, and hepatic and vascular lipid deposition using histological staining techniques. The results showed that the cholesterol-enriched diet induced alterations consistent with an early pro-atherogenic state, including increased granulocyte accumulation in the vascular region, enhanced hepatic and vascular lipid deposition, vascular morphometric changes, and trends toward elevated biochemical markers related to inflammation and lipid metabolism. In contrast, treatment with aloe-emodin significantly reduced granulocyte infiltration and lipid deposition, while attenuating several biochemical alterations induced by the hypercholesterolemic diet. Overall, these findings suggest that aloe-emodin modulates inflammatory and metabolic processes involved in early atherogenesis, highlighting its potential as a bioactive compound for preventive strategies against cardiovascular diseases.
Description
Tesis presentada para optar al grado de Magíster en Bioquímica Clínica e Inmunología.
Keywords
Arteriosclerosis, Enfermedades cardiovasculares, Pez cebra