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ABSTRACT
We aimed to evaluate the protective effects of ulinastatin (UTI) on rats with acute lung injury induced by lipopolysaccharide (LPS) via the Toll like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88)/nuclear factor-kappa B (NF-κB) signaling pathway. Forty-eight male Wistar rats were randomly divided into model, control, dexamethasone (DXM) and UTI groups. The body weight loss ratio and wet-to-dry weight ratio (W/D) of lung tissue were calculated at 10 h. The permeability of pulmonary vascular endothelium was detected by Evans blue method. Tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and IL-1β levels in bronchial lavage fluid were detected by enzyme-linked immunosorbent assay. Total cells and neutrophils were counted by microscopy. TLR4, MyD88 and NF-κB expressions were detected by Western blotting. Compared with model group, DXM and UTI groups had significantly higher body weights and lower W/D values (P < 0.05). In DXM and UTI groups, the lung tissue structure was close to normal, inflammatory cell infiltration was alleviated, and hematoxylin-eosin staining scores were significantly lower than that of model group (P < 0.05). Compared with model group, the concentrations of Evans blue, IL-1β, IL-6 and TNF-α levels, and protein expressions of TLR4, MyD88 and NF-κB in DXM and UTI groups decreased significantly (P < 0.05). UTI inhibits LPS-induced activation of the TLR4/MyD88/NF-κB signaling pathway, thereby alleviating inflammatory response and protecting against lung injury.
Highlights
Lipopolysaccharide induces activation of the TLR4/MyD88/NF-κB signaling pathway.
Ulinastatin inhibits the pathway activation.
Ulinastatin relieves inflammatory response and protects against lung injury.
Disclosure statement
No potential conflict of interest was reported by the author(s).