LIANG Xiao, LI Ang’ang, PENG Qing, LIU Jianxun, LI Junmei
China Journal of Traditional Chinese Medicine and Pharmacy. 2025, 40(4): 1686-1692.
Objective: To study the protective effect of Feiyanning (FYN) on lipopolysaccharide (LPS)-induced acute lung injury (ALI) and explore its possible mechanism. Methods: Seventy-two BALb/c mice were randomly divided into normal group, model group, FYN low-dose (0.36 g/kg) group, FYN medium-dose (0.71 g/kg) group, FYN high-dose (1.42 g/kg) group and dexamethasone group (5 mg/kg), 12 in each group. The ALT model was prepared by nasal drops of LPS in the other groups. After 30 min, the mice in the groups were given the drug according to the dosage. After 24 h of model making, the lung index, lung wet-dry weight ratio of the mice in the groups were detected, and arterial blood PO2 and PCO2 were detected. The total number of leukocytes, total protein concentration and the levels of tumor necrosis factor-α (TNF-α), interleukin (IL)-1β and IL-6 in bronchoalveolar lavage fluid (BALF); The pathological changes of lung tissue were observed by HE staining. Western Blot was used to detect HMGB-1/MyD88/NF-κB signaling pathway related protein expression in lung tissues of mice in each group. Results: Compared with the normal group, the lung index and lung wet-to-dry weight ratio in the model group were significantly increased (P<0.01, P<0.05), while arterial blood PO2 was significantly decreased and PCO2 was significantly increased (P<0.01). Pathological changes such as thickening of alveolar septa, hemorrhage, edema, and inflammatory cell infiltration were observed in the lung tissue, and the lung tissue pathological score was significantly increased (P<0.01). The levels of white blood cell count, total protein concentration, and pro-inflammatory cytokines TNF-α, IL-6, and IL-1β in BALF were significantly increased (P<0.01). The expression of HMGB1, MyD88, and p-NF-κB proteins in the lung tissue of the model group was also increased (P<0.01, P<0.05), the expression of NF-κB protein was significantly decreased (P<0.05). Compared with the model group, the low, medium, and high dose groups of FYN significantly improved the lung index, and hypoxemia in ALI mice, improved lung tissue pathological changes, and significantly reduced the total cell count, total protein concentration, levels of TNF-α, IL-6, IL-1β in BALF, and downregulated the expression, and p-NF-κB proteins in the lung tissue (P<0.05, P<0.01), the expression of NF-κB protein was significantly increased (P<0.01, P<0.05). Additionally, FYN low- and medium-dose group significantly inhibited the protein expression of HMGB1 and MyD88 in lung tissue of ALI mice (P<0.01). Conclusion: FYN can significantly improve LPS-induced ALI, and its mechanism of action may be related to downregulating the expression of HMGB1, inhibiting the activation of the MyD88/NF-κB signaling pathway, reducing the release of inflammatory factors, improving lung tissue damage, and playing a protective role in the lung tissue.
