Abstract:

Objective   To investigate the protective effect of urinary trypsin inhibitor (UTI) on lungs of septic rats, so as to provide theoretical basis for clinical treatment. Methods   The sepsis model was established by cecum ligation and puncture(CLP), and the UTI group received an intravenous administration of 5×104U/kg at 0h and 12h after the operation, while the model group and sham operation group were given the same amount of saline. 24h after the operation, rats were killed to collect the lungs and plasma specimen. The arterial blood gas and lactic acid were measured. The expression of TNF-α and IL-1β in the plasma were detected by ELLSA. The pathological changes of the lung tissue were demonstrated by HE staining. Chemical colorimetry method was used to determine the levels of SOD and MDA in the lung tissue. The apoptotic cells were detected by TUNEL method. The NF-κB mRNA expression was examined by real-time fluorescence quantitative PCR. Results   The survival rate of rats in UTI group was higher than that in model group (χ2=1.669，P>0.05).  HE staining showed the pulmonary pathological changes were attenuated in the UTI group compared with the model group, and the lung injury scores were decreased (t=5.285， P<0.01). The levels of TNF-α and IL-1β in the plasma were lower in the UTI group than that in model group (t=8.926， P<0.01； t=10.105， P<0.01).  Compared with the model group, the activity of SOD was higher in UTI group (t=5.440， P<0.01), and the level of MDA was lower (t=6.632， P<0.01). The number of apoptosis cells in the lung tissue was significantly decreased in UTI than that in the model group (t=7.539， P<0.01). The NF-κB mRNA expression was down regulated in the UTI group compared with the model group (t=3.276， P<0.01). Conclusion   UTI can play a protective role in acute lung injury resulting from sepsis. NF-κB signal pathway might participate in restraining the inflammatory responses, inhibiting the oxidation stress, and reducing the apoptosis in lung tissue.

Key words: Trypsin inhibitors; Sepsis; Lung; NF-kappa B; Apoptosis