Ameliorative Effect and Mechanism of Qingwen Baiduyin on Lipopolysaccharide-induced Acute Lung Injury / 中国实验方剂学杂志
Chinese Journal of Experimental Traditional Medical Formulae
; (24): 1-13, 2023.
Article
en Zh
| WPRIM
| ID: wpr-976534
Biblioteca responsable:
WPRO
ABSTRACT
To investigate the therapeutic effect and mechanism of Qingwen Baiduyin on acute lung injury (ALI) in mice induced by lipopolysaccharide (LPS). MethodA total of 144 C57BL/6 mice were randomly divided into the following groups: a normal group, a model group (LPS, 5 mg·kg-1), a dexamethasone group (5 mg·kg-1), and low-, medium-, and high-dose Qingwen Baiduyin groups (14.105, 28.21, 56.42 g·kg-1). The mice were treated once daily for 5 days. One hour after the final administration, the ALI model was established by intratracheal instillation of LPS, and samples were collected at 6 h and 24 h after modeling. The arterial blood gas index of mice was analyzed. The total protein content, total cell count, Evans blue dye (EBD) content, and lung tissue wet-to-dry weight ratio (W/D) of bronchoalveolar lavage fluid (BALF) were measured. Hematoxylin-eosin (HE) staining was performed to assess the pathological changes in mouse lung tissue. Western blot was used to detect the expression levels of key proteins in the Janus kinase 1/signal transducer and activator of transcription 1/interferon regulatory factor 1 (JAK1/STAT1/IRF1) signaling pathway in lung tissue. ResultCompared with the normal group, the model group showed reduced arterial oxygen pressure (pO2), oxygen saturation (SO2), and lung tissue W/D (P<0.05, P<0.01), increased carbon dioxide pressure (pCO2), total protein content, total cell count, EBD content, interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), chemokine CXC ligand 1 (CXCL1), chemokine CXC ligand 2 (CXCL2), chemokine CXC ligand 9 (CXCL9), and chemokine CXC ligand 10 (CXCL10) content (P<0.05, P<0.01), thickening of the alveolar walls, fusion of alveolar cavities, and infiltration of inflammatory cells in lung tissue, increased proportion of M1 macrophage polarization and lung cell apoptosis (P<0.05), and increased protein expression levels of JAK1, phosphorylated JAK1 (p-JAK1), inducible nitric oxide synthase (iNOS), STAT1, phosphorylated STAT1 (p-STAT1), IRF1, gasdermin D (GSDMD), and mixed lineage kinase domain-like protein (MLKL) (P<0.05, P<0.01). Compared with the model group, Qingwen Baiduyin significantly increased pO2, SO2, and lung tissue W/D (P<0.05, P<0.01), improved the pathological changes in lung tissue, and reduced pCO2, total protein content, total cell count, EBD content, IFN-γ, TNF-α, IL-1β, CXCL1, CXCL2, CXCL9, and CXCL10 content, proportion of M1 macrophage polarization, and protein expression levels of JAK1, p-JAK1, iNOS, STAT1, p-STAT1, IRF1, GSDMD, and MLKL (P<0.05, P<0.01). ConclusionQingwen Baiduyin can improve the lung inflammatory response and reduce lung cell apoptosis in mice with ALI by inhibiting the JAK1/STAT1/IRF1 signaling pathway, thereby exerting a lung-protective effect.
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Banco de datos:
WPRIM
Idioma:
Zh
Año:
2023
Tipo del documento:
Article