2021, Número 3
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Rev Biomed 2021; 32 (3)
El tratamiento con resiniferatoxina exhibe propiedades antiinflamatorias en un modelo murino de inflamación inducida por lipopolisacárido
Muñoz-Carrillo JL, Villalobos-Gutiérrez PT, Puebla-Pérez AM, López-Luna A, Flores-de la Torre JA, Alvarez-Barreto I, Gutiérrez-Coronado O
Idioma: Español
Referencias bibliográficas: 40
Paginas: 137-146
Archivo PDF: 1177.46 Kb.
RESUMEN
Introducción. La inflamación es una respuesta
fisiológica protectora del sistema inmunológico
frente a diversos estímulos, tales como la infección
o daño celular, la cual, al no resolverse de manera
adecuada, puede ser perjudicial para le hospedero.
En la búsqueda de nuevas alternativas terapéuticas
que inhiban la respuesta inflamatoria, diversos
estudios han reportado el uso de varias moléculas,
tales como la resiniferatoxina (RTX), un potente
agonista del receptor de potencial transitorio
vanilloide (TRPV)-1.
Objetivo. Evaluar si el tratamiento con RTX exhibe
propiedades antiinflamatorias, utilizando un modelo
murino de inflamación inducida por lipopolisacárido
(LPS).
Material y métodos. Se estimularon ratones
BALB/c con LPS y posteriormente fueron tratados
con dexametasona (DEX), capsaicina (CAP), Bay
11-7082, capsazepina (CPZ) y RTX. Además, otros
grupos de ratones fueron estimulados con LPS y luego
tratados con Bay 11-7082 y CPZ más RTX. Después
del tratamiento, se determinaron cuantitativamente
los niveles plasmáticos de prostaglandina (PG)-E
2,
óxido nítrico (NO), interleucina (IL)-1β y factor de
necrosis tumoral (TNF)-
α utilizando kits de
Enzyme-
Linked ImmunoSorbent Assay ELISA.
Resultados. El tratamiento con RTX disminuyó
de manera significativa los niveles plasmáticos de
PGE
2, NO, IL-1β y TNF-
α. Así mismo, se observó
que los tratamientos con Bay 11-7082 y CPZ más
RTX mostraron un efecto antiinflamatorio sinérgico,
observándose una disminución significativa más
pronunciada en los niveles plasmáticos de TNF-
α
y PGE
2.
Conclusión. Estos hallazgos sugieren que el
tratamiento con RTX muestra propiedades
antiinflamatorias, aparentemente asociadas con
la vía de señalización factor nuclear (NF)-κB,
independiente de los receptores TRPV1, colocando a
la RTX como un fármaco potencial en el tratamiento
de enfermedades inflamatorias
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