| Objectives:1.To establish a research platform for animals of inhalation injury caused by black gunpowder smog.2.To establish and evaluate a rat model of inhalation lung injury caused by black gunpowder smog.3. To examine the interventional effects of ulinastatin (UTI) on inhalation lung injury caused by black gunpowder smog in rats.Methods:1.A smog-generating device was designed and the smog composition was measured. The relationship between mortality rate and gunpowder dosage, smog-exposure time was studied.2. Forty two healthy male Wistar rats were randomly divided into a normal control group (Group C) and inhalation groups which were further divided into1h,2h,6h,24h,48h and96h subgroups (Group I-1h,I-2h,I-6h,I-24h, I-48h,I-96h). Rats in inhalation groups were exposed to smog generated by10g gunpowder for8min. The blood gas values, coagulation function, lung wet to dry weight ratio (W/D), white blood cells count (WBC), protein concentration in bronchoalveolar lavage fluid (BALF) and myeloperoxidase (MPO) in serum were assayed. Pathological evaluation of pulmonary was performed.3. Thirty healthy male Wistar rats were randomly divided into a normal control group (Group C), an inhalation group (Group I) and a100000U/(kg-d) UTI group (Group UH), a50000U/(kg·d) UTI group (UM group) and a20000U/(kg·d) UTI group (UL group). There were6rats in each group and the rats except those in the control group were exposed to smog generated by10g gunpowder for8min.40h after exposed to smog, the blood gas values, W/D, WBC and protein concentration in BALF were tested, while MPO activity in serum and lung tissue, malondialdehyde (MDA) concentration, pathological evaluation of lung were also assayed. The Messenger ribonucleic acid (mRNA) expression of toll-like receptor4(TLR-4), Interleukin-1β (IL-1β), Tumor necrosis factor-α (TNF-α) were detected by reverse transcription fluorescence quantitative polymerase chain reaction (PCR). Results:1.The smog composition mainly included CO2and CO which remained stable for12minutes. As gunpowder dosage and exposure time increased, the mortality increased.2. Smog inhalation caused a significant hypoxemia. The value of Carboxyhemoglobin (COHb) increased after1h post-injury (P<0.05), results of coagulation function showed no significant difference (P<0.05) and lung W/D peaked at2h (P<0.05). WBC and protein concentration in BALF both increased significantly within24h post-smog inhalation (P<0.05). MPO activity in serum increased within48h post-smog inhalation (P<0.05). Histopathological observation exhibited that there were inflammatory exudates and diffuse hemorrhage in the lung tissue with significant edema, which did not recover at96h.3. The value of partial pressure of oxygen (PaO2) in UH, UM, UL groups were higher than that in I group (P<0.05), while W/D, WBC counts in these three groups were lower than I group (P<0.05). There was no significant difference in partial pressure of carbon dioxide (PaCO2) and protein concentration among UH, UM, UL groups and C group (P>0.05). MPO activity in serum and lung, MDA concentration in UH group were both lower than those in I group (P<0.05). High-dose UTI significantly inhibited the mRNA expressions of IL-1β and TNF-α while middle-dose and low-dose can only inhibited the mRNA expression of IL-1β (P<0.05). Histopathology results exhibited that there were less inflammatory exudates and infiltrations in three UTI treated groups than I group.Conclusions:1.The research platform is estabilished, which is an economical, convenient apparatus and simply to operate.2. The rat model caused by black gunpowder smog is established and it has the advantages, such as easy-repeatable, reliable performance and stability.3. UTI shows the protective effects on rats of inhalation lung injury caused by black gunpowder smog through the mechanism of anti-inflammation and anti-oxidation by reducing the levels of MPO, MDA and inhibiting the mRNA expressions of IL-1β and TNF-α. |
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