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Regresión de la aterosclerosis: papel del óxido nítrico y la apoptosis
1Section of Vascular Medicine, Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, Calif, USA.
Circulation
|March 9, 1999
Resumen
La L-arginina suplementaria induce la apoptosis de los macrófagos en las lesiones ateroscleróticas al aumentar los niveles de óxido nítrico (NO). Esto sugiere una estrategia terapéutica potencial para la aterosclerosis mediante la manipulación de la vía de la NO sintasa.
Área de la Ciencia:
- Investigación cardiovascular Investigación cardiovascular Investigación cardiovascular Investigación cardiovascular Investigación cardiovascular
- Biología celular Biología celular.
- La bioquímica es la bioquímica.
Sus antecedentes:
- La administración de L-arginina promueve la regresión de las lesiones ateroscleróticas en conejos con hipercolesterolemia.
- La activación de la vía de la síntesis de óxido nítrico (NO) puede inducir la apoptosis de las células vasculares in vitro.
Objetivo del estudio:
- Para determinar si la suplementación dietética de L-arginina induce apoptosis en lesiones ateroscleróticas íntimas.
- Investigar si este efecto apoptótico está mediado por la vía de la NO sintasa.
Principales métodos:
- Los conejos con hipercolesterolemia fueron alimentados con una dieta de colesterol y suplementados con L-arginina.
- Los segmentos aórticos se analizaron ex vivo con moduladores de la vía de la NO sintasa.
- La apoptosis se evaluó histológicamente y se midieron los óxidos de nitrógeno.
Principales resultados:
- El tratamiento con L-arginina aumentó las células apoptóticas (principalmente macrófagos) en lesiones íntimas tres veces.
- El nitroprussido de sodio y la L-arginina aumentaron la apoptosis y la liberación de óxido de nitrógeno.
- Estos efectos fueron antagonizados por un inhibidor de la NO sintasa y no imitados por la D-arginina.
Conclusiones:
- La L-arginina suplementaria induce la apoptosis de los macrófagos en lesiones ateroscleróticas a través de la producción de NO a través de una vía independiente del cGMP.
- Estos hallazgos apoyan las observaciones anteriores del papel de la L-arginina en la regresión del ateroma.
- El estudio proporciona una justificación para explorar la manipulación de la vía de la NO sintasa en el tratamiento de la aterosclerosis.
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