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La 3,6'-Disinapoyl sacarosa modula la reprogramación metabólica mediada por GALE para aliviar la inflamación de las
Haisong Jiang1, Ningpo Ding2, Zongqi Wang2
1Department of Anesthesiology, Yanbian University Medical College, Yanji 133002, PR China; Jilin Key Laboratory for Immune and Targeting Research on Common Allergic Diseases, Yanbian University, Yanji 133002, PR China.
International immunopharmacology
|September 4, 2025
Resumen
Este estudio revela que la UDP-galactosa-4-epimerasa (GALE) es un factor metabólico clave en el asma. El compuesto natural 3,6'-Disinapoyl Sucrose (DISS) tiene como objetivo GALE para reducir la inflamación de las vías respiratorias y la disfunción metabólica.
Área de la Ciencia:
- Metabolomía y Biología de Sistemas
- Mecanismos moleculares de las enfermedades respiratorias
- Intervenciones farmacológicas para el asma
Sus antecedentes:
- El asma implica inflamación crónica de las vías respiratorias y desregulación metabólica, con fundamentos moleculares poco claros.
- Los desequilibrios en la glucólisis y la fosforilación oxidativa (OXPHOS) están implicados en la patogénesis del asma.
- La UDP-galactosa-4-epimerasa (GALE), crucial para el metabolismo de la galactosa, no ha sido estudiada en el asma.
Objetivo del estudio:
- Identificar los genes metabólicos asociados con el asma utilizando la bioinformática.
- Investigar el papel de la UDP-galactosa-4-epimerasa (GALE) en el asma.
- Evaluar el potencial terapéutico de 3,6 -Disinapoyl Sucrose (DISS) en la modulación de la reprogramación metabólica mediada por el GALE.
Principales métodos:
- El análisis ponderado de la red de coexpresión génica (WGCNA) y el aprendizaje automático identificaron GALE a partir de conjuntos de datos epiteliales bronquiales.
- El cribado virtual identificó a DISS como un inhibidor de GALE.
- Los experimentos in vitro (células BEAS- 2B) e in vivo (modelo de ratón con asma inducida por HDM) evaluaron la eficacia del DISS.
Principales resultados:
- La expresión de GALE se correlacionó con los subtipos de asma severa y neutrófila.
- DISS suprimió la glucólisis, restauró el equilibrio redox y mitigó la disfunción mitocondrial in vitro.
- DISS atenuó la inflamación de las vías respiratorias, la hipersecreción de moco y la remodelación de las vías respiratorias in vivo.
Conclusiones:
- La reprogramación metabólica impulsada por GALE representa un nuevo mecanismo en la progresión del asma.
- DISS demuestra potencial terapéutico al dirigirse a GALE, normalizando la glucólisis y reduciendo el estrés oxidativo.
- DISS ofrece una estrategia prometedora para el tratamiento del asma al abordar la desregulación metabólica.
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