AIMTo explore the effects of aminoguanidine (AG) inhalation on bleomycin (BLM)-induced fibrosis in lungs of rats and its possible mechanism.

METHODSSixty male Sprague-Dawley rats were randomly divided into 4 groups: BLM plus normal saline (NS) group, BLM plus 10 mmol/L AG group, BLM plus 50 mmol/L AG group, and NS plus NS group. At the same day when administrated by single intratracheal instillation of BLM (5 mg/kg) or equal volume of NS as control, the rats received NS (the same volume as AG) or AG inhalation (10 mmol/L AG, or 50 mmol/L AG, 5 min/each time, 2/day) for 30 d. The nitrite/nitrate (NO2-/NO3-) content of plasma in pulmonary artery, hydroxyproline content and the pathological changes in lungs, as well as lipid peroxide (LPO) content of plasma in pulmonary artery were examined.

RESULTSThe NO2-/NO3- content of plasma in pulmonary artery was increased in rats on day 14 after intratracheal instillation of BLM, compared with that of the control rats (P < 0.01). The hydroxyproline content in lung, the grade of pulmonary alveolitis and the content of LPO of plasma in pulmonary artery were increased in rats on day 30 after intratracheal instillation of BLM, compared with that of the control rats, respectively (P < 0.05, P < 0.01, P < 0.01). The above-mentioned changes were ameliorated by AG inhalation (10 mmol/L AG, or 50 mmol/ LAG, 5 min/each time, 2/day) for 30 d (P < 0.01, P < 0.05, P < 0.05, P < 0.01).

CONCLUSIONAG inhalation has anti-action on BLM-induced fibrosis in lung, which might be related to blockage of oxidative injury in lung.