Pre-B cell colony enhancing factor (PBEF) is recognized as a proinflammatory cytokine involved in acute lung injury, but its contribution to lung damage following cardiopulmonary bypass (CPB) has not been clarified. This study explored how reducing PBEF expression affects lung injury and the regulation of sodium and water transport in a rat model of CPB. Lung morphology was examined using hematoxylin and eosin staining. Immunohistochemistry was applied to assess PBEF levels. Western blotting was used to measure proteins related to sodium–water balance and to analyze associated signaling pathways. Rats subjected to CPB displayed marked alveolar wall injury and increased free PBEF levels compared with controls. CPB also led to elevated expression of PBEF, surfactant protein D, aquaporin 1, aquaporin 5, and the epithelial sodium channel. Administering an adenovirus carrying sh-PBEF lowered the expression of these proteins in CPB-treated rats. In addition, phosphorylation of ERK1/2, AKT, and p38 MAPK was heightened after CPB but decreased following sh-PBEF treatment. Delivering sh-PBEF through an adenoviral vector may help lessen CPB-induced lung damage and improve sodium and water transport in the lungs, possibly by suppressing MAPK, ERK1/2, and AKT signaling pathways.
