RESUMEN

OBJECTIVE: To explore the effect and mechanism of baicalin in the treatment of acute lung injury (ALI) by and experiments. METHODS: ALI was induced by instilling 10 mg/mL lipopolysaccharide (LPS) into the airway of rats. Different doses of baicalin (50 and 100 mg·kg ·d) were administered by gavage one day before modeling. RESULTS: Baicalin significantly reduced the permeability of the alveolocapillary membrane, alleviated tissue injury and inflammatory infiltration, and inhibited the secretion of inflammatory factors and the infiltration of neutrophils. The decline in these inflammations was related to the inhibition of the toll like receptor-4 (TLR4)/myeloid differentiation factor 88 (MyD88)/nuclear factor-kappa B (NF-κB)/nod-like receptor pyrin containing 3 (NLRP3) signaling pathway and the mitogen-activated protein kinase (MAPK) signaling pathway. CONCLUSIONS: Baicalin inhibits the secretion of inflammatory factors by inhibiting the TLR4-MyD88-NF-κB/NLRP3 pathway and the MAPK signaling pathway. Thus, it reduces lung bronchial epithelial layer, alveolar damage, and pulmonary edema as detected in the and experiments. Therefore, baicalin may be a potential preventive and therapeutic drug for ALI.

Asunto(s)

Lesión Pulmonar Aguda , Lipopolisacáridos , Lesión Pulmonar Aguda/inducido químicamente , Lesión Pulmonar Aguda/tratamiento farmacológico , Lesión Pulmonar Aguda/genética , Animales , Flavonoides , Humanos , Inflamación/tratamiento farmacológico , Lipopolisacáridos/efectos adversos , Factor 88 de Diferenciación Mieloide/genética , Factor 88 de Diferenciación Mieloide/metabolismo , FN-kappa B/genética , FN-kappa B/metabolismo , Proteína con Dominio Pirina 3 de la Familia NLR/metabolismo , Ratas , Transducción de Señal , Receptor Toll-Like 4/genética , Receptor Toll-Like 4/metabolismo