动物造模,幼鼠急性肺损伤 z-bio 2022-02-06 664

　　Objective To explore the role of astragaloside IV mediated TLR4-p38 MAPK signaling pathway in a rat model of acute lung injury.

　　Methods 7-day-old SD neonatal rats were used as experimental subjects. Lipopolysaccharides were used to construct an acute lung injury model of juvenile rats. Dexamethasone was used as a positive drug control. Each juvenile was injected intraperitoneally with 10 mL/kg astragaloside IV. Observation of lung tissue lesions at 12 h and 24 h, detection of TLR4, p-p38 protein and mRNA expression, TNF-α, IL-6, IL-12 inflammatory factors mRNA expression changes.

　　Results The model group showed pulmonary hemorrhage 12 hours after modeling, a large number of alveolar collapsed, 24 hours showed pulmonary edema, and the alveolar interval was significantly widened. Compared with the model group, the lung tissue lesions of the astragaloside IV group were significantly reduced. In addition, the protein detection results showed that compared with the model group, the expression of TLR4 and p-p38 protein in the astragaloside IV group was significantly reduced (P<0.05, P<0.001) q-PCR results showed that compared with the model group, The relative expression of TLR4 mRNA in the Astragaloside IV group was significantly reduced, and there was a significant difference from the model group (P<0.05). The inflammatory factors of TNF-α, IL-6 and IL-12 all have a downward trend, and the relative expression of IL-12 is significantly different from that of the model group (P<0.05).

　　Conclusion Astragaloside IV plays an important role in the acute lung injury model of young rats by inhibiting the TLR4-p38 MAPK signaling pathway.