关键词: 双氢杨梅树皮素, TLR4, MyD88, NF-κB, 炎症, 急性肺损伤

Abstract: Aiming to investigate the effects of ampelopsin （APS） on lipopolysaccharide （LPS）-induced acute lung injury in mice and its underlying mechanism, the acute lung injury mouse model was established by intratracheal instillation of LPS. Seventy-two KM mice were randomly divided into 6 groups as follows： normal, model, dexamethasone and APS high-dosage, medium-dosage, and low dosage group. After 8 h of LPS induction, the animal lung function analysis system was employed to monitor pulmonary function （airway resistance, pulmonary dynamic compliance and minute ventilation volume） of mice. ELISA assay was carried out to measure the content of inflammatory factors TNF-α and IL-1β. Colorimetric assay was performed to determine MPO activity. H&E staining was performed to reveal pathological changes in lung tissues. Western blotting was performed to measure the protein expression of TLR4, MyD88, IκBα, p-IκBα, p65 and p-p65. Results showed that APS administration decreased airway resistance and increased pulmonary dynamic compliance and minute ventilation volume compared to those in the model group. Also, APS reduced TNF-α, IL-1β content and MPO activity. Further, Western blotting results demonstrated that APS down-regulated the protein expression of TLR4, MyD88, p-IκBα, p65 and p-p65, and up-regulated IκBα protein expression in LPS-induced acute lung injury. APS exerted a protective effect on LPS-induced acute lung injury in mice through regulating the TLR4/MyD88/NF-κB signaling pathway.

Key words: ampelopsin, TLR4, MyD88, NF-κB, inflammation, acute lung injury