Objective：To observe the changes and significances of aquaporin 5（AQP5） and matrix metalloproteinases-9（MMP-9） in severe acute pancreatitis（SAP） associated with lung injury. Methods：SAP model was prepared through retrograde injection of 5% taurocholic acid. SD rats were randomly divided into SAP group and shamed-operated（SO） group. Lung structure damage and AQP5，MMP-9 expressions in lung tissues were examined at 3，6，12 h and 24 h during disease development through the immunofluores－cence staining，real-time PCR and Western blot analysis. Results：Lung tissues were significantly damaged in SAP group compared with those in SO group. Immunofluorescence staining，real-time PCR and Western blot showed that in SAP group，there was no change in AQP5 expression until 3 h（P >0.05） and it was gradually decreased at 6 h afterwards（P<0.05）；in SAP group，MMP-9 mRNA ex－pression was significantly increased at 3 h afterwards and was reached the peak at 12 h（P<0.05） but was gradually decreased at 24 h afterwards. MMP-9 protein expression was gradually increased at 3 h afterwards（P<0.001）. Conclusions：AQP5 expression remains constant in lung tissue at early stage of SAP associated with lung injury，but decreases at later stage. This indicates that AQP5 may not be the direct reason for early edema of lung injury. Large expression of MMP-9，pulmonary capillaries basement membrane dissolution，discontinuity and increase of blood capillary permeability are perhaps the main mechanisms of early edema of lung injury. But the decreased lung AQP5 expression can affect the efficiency of transmembrane transport of water molecule mediated by AQP5，induce alveoli liquid removing obstacles and promote the formulation of lung endema，which will increase the severity of lung edema and propel the process of acute respiratory distress syndrome.