Protective effects of ulinastatin on phosgene-induced acute lung injury and the expression of tumor necrosis factor-alpha / 中华急诊医学杂志

ABSTRACT

Objective To observe the effects of ulinastatin on the expressions of tumor necrosis factor-α (TNF-α) in the lung tissues of rats with acute lung injmy induced by phosgene, and to explore the mechanism of ulinastafin in treating acute lung injury. Method Sixty-four clean grade healthy male SD rots were randomly divided(random number) into eight groups with eight in each group. Group A1 in which rats were exposed to air. Group A2 in which rots wereexposed to air and treated with saline. Group A3 in which rats were exposed to air and treated with dexamethasone. Group A4 in which mrs were exposed to air and treated with ulinastatin. Group B1 in which rots were exposed to phosgene without treatment. Group B2 in which rats were exposed to phosgene and treated with saline. Group B3 in which rats were exposed to phosgene and treated with dexamethasone. Group B4 in which rats were exposed to phosgene and treated with ulinastatin. The expressions of TNF-α in the lung tissues were measured by using immunohistocheistry. Lung tissues were observed grossly and under 200-fold light microscope to identify the positive expressions in kytoplasm. Results In group B1 and group B2, the wet weight, dry weight and wet/dry weight ratio og right lower lobe of lung were higher thai those in group A1 and group A4( P <0.01 ), and those in group B4 and group B3 were significantly lower than those in group B1(P<0.01 ), but still higher than those in group A1 and A4(P<0.01). The gross observation suggested that the surfaces of lung tissues in group A1and group A2 were slick and rose pink without congestion, dropsy or infarction; the surfaces of lung tissue in groups B1 and B2 appeared with congestion, dropsy and many petechia. The surfaces of lung tissue in groups B3 and B4 were similar to those in groups B1 and B2. Under the light microscope, the structure, of lungs in groups A1 and A2 were clear without congestion, effusion or inflammatory cell infiltration. In groups B1 and B2, the engorgement of lung capillary vessels, congestion and tiny thrombosis were found and there abundant edematous fluid and inflammatory cell infiltration in lung stroma and alveolus with focal pulmonary atelectasis in some lung tissue section. The tissues in groups B3 and B4 showed congestion, dropsy, tiny thrombosis and inflammatory cell infiltration, but these changes were slighter than those in groups B1 and B2. The expressions of TNF-α in groups B1, B2, B3, and B4 were significantly higher thanthose in groups A1 and A2( P < 0.01 ), but the expressions of TNF-α IN group B4 was lower than that in groups B1 and B2(P<0.01). Conclusions Ulinastatin could lessen the lung injury by reducing the expressions of pro-inflammatory cytokines such as TNF-α.