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BACKGROUND: Ultrashort wave can inhibit the inflammatory response and is often used in symptomatic treatment of pulmonary infection. Uncontrolled inflammatory response is an important pathogenesis of acute lung injury. Inhibiting inflammation is an important strategy for controlling acute lung injury. OBJECTIVE: To observe the effects of ultrashort wave on inflammatory response and the expression of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in rats with acute lung injury. METHODS: Twenty-four 3-month-old male Sprague-Dawley rats were randomly divided into control group, acute lung injury group (model group) and ultrashort wave group (n=8 per group). Rats in the acute lung injury group and the ultrashort wave group were given intratracheal lipopolysaccharide to replicate the acute lung injury model. Rats in the control group were given intratracheal infusion of the same amount of normal saline. In the ultrashort wave group, rats were given ultrashort wave intervention immediately, 4 and 8 hours after lipopolysaccharide infusion, once for 15 minutes. Experimental animals were sacrificed 24 hours after intratracheal infusion of lipopolysaccharide or normal saline. The lung tissues of rats were compared by hematoxylin-eosin staining, lung histopathological semi-quantitative score and lung wet/dry weight ratio (W/D). Serum levels of inflammatory factors TNF-α and IL-1β were detected by ELISA, and mRNA and protein expressions of TNF-α and IL-1β were detected by RT-PCR and western blot, respectively. The study protocol was approved by the First Affiliated Hospital of Nanhua University, approved No.202002100009. RESULTS AND CONCLUSION: Lung W/D ratio in the acute lung injury group was significantly higher than that in the control group (P < 0.01), whereas the ratio in the ultrashort wave group was lower than that in the acute lung injury group, but there was no significant difference between the two groups. Pathological manifestations: In the model group, the lung tissue structure was obviously damaged, with different sizes of alveolar septa, the alveolar wall was incomplete, thickened and fractured, a large number of neutrophils were seen in the lung interstitium, and some red blood cells were exudated. In the ultrashort wave group, compared with the model group, the alveolar structure was relatively complete and clear, and the infiltration of inflammatory cells and red blood cell exudation from the lung interstitium were reduced. Semi-quantitative histopathological score of the lung was significantly higher in the model group than the control group (P < 0.01), but significantly reduced in the ultrashort wave group compared with the model group (P < 0.01). Serum TNF-α and IL-1β levels in the model group were significantly higher than those in the control group (both P < 0.01). After ultrashort wave exposure, the levels of serum TNF-α and IL-1β significantly decreased compared to the model group (both P < 0.05). After ultrashort wave exposure, the mRNA and protein expressions of TNF-α and IL-1β significantly decreased compared to the model group (P < 0.01 or P < 0.05). To conclude, ultrashort wave may inhibit the inflammatory response of the lung tissue in rats with acute lung injury by down-regulating the expression of inflammatory cytokines, TNF-α and IL-1β. [ABSTRACT FROM AUTHOR]