Induction of autophagy via the TLR4/NF-κB signaling pathway by astragaloside â
£ contributes to the amelioration of inflammation in RAW264.7 cells.
Biomed Pharmacother
; 137: 111271, 2021 May.
Article
en En
| MEDLINE
| ID: mdl-33561643
Cigarette smoking-related lung injury is one of the most common and fatal etiologies of many respiratory diseases, for which no effective interventions are available. Astragaloside â
£ (ASâ
£) is an active component extracted from Astragalus membranaceus. It is prescribed as a treatment for upper respiratory tract infections. Here, we report the potential anti-inflammatory effects and mechanisms of ASâ
£ on cigarette smoking extract- (CSE)-exposed RAW264.7 cells. Murine macrophages were exposed to CSE, followed by administration of ASâ
£ at 25-100 µg/mL for 24 h. ASâ
£ significantly rescued CSE-induced cell death by inhibition of release pro-inflammatory cytokines. We measured autophagy as an intracellular scavenger by analyzing autophagic flux using tandem mRFP-GFP-LC3 fluorescence microscopy. Following administration with ASâ
£ in CSE-exposed RAW264.7 cells, there was a notable increase in autophagosomes and a range of autophagic vacuoles were generated, as seen with transmission electron microscopy. Loss of autophagy following transfection siRNA aggravated inflammatory injury and release of inflammatory cytokines. Mechanistically, ASâ
£-triggered autophagy is mediated by the TLR4/NF-κB signaling pathway to reduce inflammation. Taken together, our findings suggest that ASâ
£ acts stimulates autophagy, and that ASâ
£ induces autophagy by inhibiting the TLR4/NF-κB signaling pathway, contributing to alleviation of inflammation.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Saponinas
/
Autofagia
/
Triterpenos
/
FN-kappa B
/
Receptor Toll-Like 4
/
Inflamación
/
Macrófagos
/
Antiinflamatorios
Límite:
Animals
Idioma:
En
Revista:
Biomed Pharmacother
Año:
2021
Tipo del documento:
Article
País de afiliación:
China