OBJECTIVE: To probe into the protective mechanism of ulinastatin on early radiation-induced pulmonary injury based on the signal pathway of high mobility group box-1 protein（ HMGB1）. METHODS: 36 SD rats were divided into normal control group

radiation-induced pulmonary injury group and ulinastatin group according to different intervention methods

with 12 cases in each group. The bronchoalveolar lavage fluid（ BALF） and lung tissue of rats in each group were collected

the lung tissue was stained with hematoxylin-eosin so as to observe its morphological change. Ray-giemsa staining method was adopted to measure various white blood cells counts in BALF

Western blotting method was adopted to measure the expression levels of HMGB1 protein and downstream gene protein in lung tissue

real-time fluorescence quantification polymerase chain reaction was adopted to measure the expression levels of HMGB1 and downstream gene mRNA in lung tissue. RESULTS: There was no inflammatory cell infiltration in the bronchus

submucosa and pulmonary interstitium of rats in normal control group; while there was a large number of inflammatory cells infiltrated in the bronchus

submucosa and pulmonary interstitium of rats in the radiation-induced pulmonary injury group

with pulmonary interstitial thickening; the number of inflammatory cells in bronchi

submucosa and pulmonary interstitium of rats in the ulinastatin group was significantly less than that of the radiationinduced lung injury group

and pulmonary interstitial edema was significantly alleviated; compared with normal control group

the proportions of eosinophilic granulocyte

neutrophile granulocyte

lymphocyte and monocyte in the BALF of rats in radiation-induced pulmonary injury group and ulinastatin group were increased

the protein expression levels of HMGB1

receptor for advanced glycation end products（ RAGE）

nuclear transcription factor-κB（ NF-κB）

tumor necrosis factor α（ TNF-α）

interleukin-6（ IL-6） and interleukin-1β（ IL-1β） were increased

the mRNA expression levels of HMGB1

RAGE

NF-κB

TNF-α

IL-6 and IL-1β were increased

with statistically significant differences（ P<0. 05）; compared with radiation-induced pulmonary injury group

the proportions of eosinophilic granulocyte

neutrophile granulocyte

lymphocyte and monocyte in the BALF of rats in ulinastatin group were decreased

the protein expression levels of HMGB1

RAGE

NF-κB

TNF-α

IL-6 and IL-1β were decreased

the mRNA expression levels of HMGB1

RAGE

NF-κB

TNF-α

IL-6 and IL-1β were decreased

with statistically significant differences（ P <0. 05）. CONCLUSIONS: Ulinastatin can relieve pulmonary inflammatory infiltration in rats with early radiation-induced pulmonary injury by interrupting HMGB1 signaling pathway by reducing the expression of HMGB1 and its downstream protein

which is likely to be a drug to prevent and treat early radiation-induced pulmonary injury.