动物造模,急性肺损伤 z-bio 2022-02-17 282

　　Objective: To observe the effect of Xuanfei Decoction on the mTOR/S6K1 signaling pathway of endotoxin-induced acute lung injury in rats, and to explore its mechanism of action.

　　METHODS: Thirty male Wistar rats were selected, and the animals were randomly divided into normal group, model group, dexamethasone group and Xuanfeifang group (high and low dose groups). ALI model was prepared by injecting LPS into tail vein. The contents of inflammatory factors TNF-α, IL-1β and IL-6 in bronchoalveolar lavage fluid (BALF), the expression of mTOR protein was measured by immunohistochemistry, the expression of p-mTOR protein in lung tissue was measured by Western blot, and the expression of p-mTOR protein in lung tissue was measured by RT-PCR. The expression of RPS6KB1 gene in phagocytes was observed, and the pathological changes of rat lung tissue were observed.

　　Results: Compared with the normal group, TNF-α, IL-1β, IL-6, RPS6KB1 in the model group were significantly increased (P<0.05), and the positive area rate of mTOR protein and the expression of p-mTOR protein were significantly decreased (P<0.0 P <0.05); compared with the model group, TNF-α, IL-1β, and IL-6 in the dexamethasone group were significantly decreased (P<0.05); the gene expression of TNF-α, IL-6, RPS6KB1 in the high-dose Xuanfei recipe group significantly decreased (P<0.0 P<0.05), the mTOR protein positive area ratio and p-mTOR protein expression were significantly increased (P<0.0 P<0.05), and the TNF-α content in the low-dose Xuanfei recipe group was significantly decreased (P<0.01). ). HE staining showed that local pulmonary hemorrhage, necrosis, dilation of pulmonary venules, significant increase in the number of leukocytes in blood vessels, pulmonary interstitial edema, and inflammatory cell infiltration were seen in the lung tissue of the model group; Qualitative pneumonia.

　　Conclusion: Xuanfei recipe has protective effect on endotoxin-induced acute lung injury in rats, and its mechanism may be related to its ability to down-regulate TNF-α, IL-6 content, RPS6KB1 gene expression and up-regulate mTOR and p-mTOR protein expression.