Protective effects of ulinastatin on rats with acute lung injury induced by lipopolysaccharide

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-kappa B) 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-alpha (TNF-alpha), interleukin-6 (IL-6) and IL-1[3 levels in bronchial lavage fluid were detected by enzyme-linked immunosorbent assay. Total cells and neutrophils were counted by microscopy. TLR4, MyD88 and NF-kappa B 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 signifi-cantly lower than that of model group (P < 0.05). Compared with model group, the concentrations of Evans blue, IL-1[3, IL-6 and TNF-alpha levels, and protein expressions of TLR4, MyD88 and NF-kappa B in DXM and UTI groups decreased significantly (P < 0.05). UTI inhibits LPS-induced activation of the TLR4/MyD88/NF-kappa B signaling pathway, thereby alleviating inflammatory response and protecting against lung injury.