RÉSUMÉ
Acute lung injury (ALI), during the progression of infectious shock, leads to systemic inflammatory response syndromewith increased pulmonary capillary membrane permeability due to pulmonary inflammation and uncontrolled inflammatoryresponses. It may cause fatality in patients. Here, we evaluated the protective effect of breviscapine on ALI in rats withinfectious shock. Sprague-Dawley (SD) rats were assigned into Sham, model [lipopolysaccharide (LPS) group], andbreviscapine treatment groups (LPS + breviscapine group) and weighed. The lung coefficient, and the wet-to-dry weightratio (W/D) and moisture content of lung tissues were calculated. The pathological changes of the lung tissues were detectedusing hematoxylin-eosin (HE) staining, and the protein expressions of interleukin-1 beta (IL-1?), IL-6, and tumor necrosisfactor-alpha (TNF-?) were determined by enzyme-linked immunosorbent assay. Western blotting was conducted to measurethe protein expressions of toll-like receptor-9 (TLR-9) and nuclear factor-kappa B (NF-?B) (p65). Compared with LPSgroup, breviscapine significantly lowered the lung coefficient and the W/D and moisture content of lung tissues, relieved thepathological changes of lung tissues, reduced the protein expression levels of IL-1?, IL-6, and TNF-?, weakened theactivation of NF-?B (p65) in lung tissues, and repressed the protein expressions of TLR-9 and NF-?B (p65).