Background  Inhalation injury is most commonly caused by heat and toxic fumes, but studies on its pathogenic mechanisms remain elusive.

  Objective  To develop a simple and easily available new mouse model of smoke inhalation injury, and observe the changes in the physiological status, histopathological and inflammatory factors of mice.

  Methods  Of the 160 57BL/6 mice, 20 mice were randomly selected as the control group, the rest of the 140 mice were randomly divided into 4 groups. Smoke inhalation injury was performed for 10, 15, 20, and 25 min using a self-made smoke injury device with plywood and pine chips as smoke materials, respectively, the control group received no special treatment, and other treatments were the same as those in each smoke inhalation group. The behavioral status, physiological performance, and 72-hour survival changes in mice after smoke inhalation injury were observed. Lung tissues were taken from mice in each group after sacrifice to observe the pathological changes, dry and wet weight changes, and detect the contents of intracellular proteins and inflammatory factors in tissue cells.

  Results  The survival rates at 72 hours post-inhalation injury for the above 10 min-, 15 min-, 20 min-, and 25 min-smoke-inhalation injury groups were 100%, 83%, 54%, and 0, respectively; and all the mice in the 25 minutes-smoke-inhalation injury group died within 12 hours after injury. Except for the control group, tachypnea and decreased activity were immediately observed after smoke inhalation injury in the live mice of each group and these abnormal signs subsided several hours later. Some mice in the experimental group showed loss of appetite and malaise. Inflammatory cell infiltration, alveolar structure destruction, and alveolar septum thickening were observed in the lung pathological tissues of mice in the 20 min smoke-inhalation injury group, and the dry and wet weight ratio showed the appearance of pulmonary edema. Interleukin-1β, 6 (IL-1β, IL-6) and tumor necrosis factor-α (TNF-α) detected by inflammatory factors in lung homogenates of mice at 12 h and 24 h after injury in the 20 min smoke-inhalation injury group increased significantly compared with the control group, while interleukin-10 (IL-10) significantly decreased (all P＜0.05).

  Conclusion  Inhalation of smoke produced by mixed combustion of plywood and pine for 20 min can lead to moderate to severe inhalation injury in C57BL/6 mice, and the physiological manifestations and histopathological results of the experimental animals after injury are consistent with the clinical condition, and the release of inflammatory mediators and cellular inflammatory factors is also significantly changed in mice after injury.