Down-regulated expression of AQP5 on lung in rat DIC model induced by LPS and its effect on the development of pulmonary edema.

Disseminated intravascular coagulation (DIC) is an acquired syndrome characterized by the widespread activation of coagulation, which leads to failure of multiple organs in the body. DIC of rat with lipopolysaccharide (LPS) is associated with subsequent pulmonary edema. Lung tissue is highly water permeable and expresses several aquaporins (AQPs). We therefore explored whether AQP5 involved in the pathogenesis of LPS-induced lung edema. The rats were intravenously infused with LPS (30 mg/kg) for 4 h, 6 h, 8 h, 10 h, and 12 h to induce DIC. Platelets count (PLT), D-Dimer (DD), fibrinogen (FIB), prothrombin time (PT), and activated partial thromboplastin time (APTT) were determined. Real-time quantitative PCR and Western blot were used to analyze the mRNA and protein expression of AQP5. Lung samples were stained with hematoxylin-eosin and lung wet/dry weight (W/D) ratios were measured. Here, we demonstrated that PLT and FIB values were significant decreased, the values for DD, PT, and APTT were marked increased, microthrombus was observed in lung specimens, and simultaneously with the AQP5 showed down-regulated expression following LPS infused from 4 h to 12 h. However, histopathological changes such as pulmonary edema and the increased lung W/D weight ratio were observed after LPS infused from 6 h to 12 h. These results indicated that the decreased expression of AQP5 maybe induce liquid transport obstacles between alveolar and capillary, and provides the report of AQP5 gene regulation, revealing the pathogenesis of pulmonary edema in DIC model of rat.