Effects of sildenafil on inflammatory injury of the lung in sodium taurocholate-induced severe acute pancreatitis rats.

• Acute lung injury occurs in sodium taurocholate-induced severe acute pancreatitis. • Sildenafil decreases inflammatory factors, neutrophils and chemokines generation. • Sildenafil could promote proliferation and inhibit apoptosis under SAP condition. • Sildenafil may enhance antioxidant (Nrf2 and HO-1) genes and suppress NF-κb. Inflammatory response and acute lung injury (ALI) occur in sodium taurocholate-induced severe acute pancreatitis (SAP). Because sildenafil has anti-inflammatory, anti-oxidant and immune-modulating effects, we investigated its effect on inflammatory and lung injury in sodium taurocholate-induced SAP-associated ALI rat lung. Sodium taurocholate-induced SAP rats received sildenafil (100 mg/kg) or not and were compared to age-matched normal control animals. We evaluated inflammatory response by detecting the expression of inflammatory factors including IL-1β, IL-6 and TNF-α, and detected the level of lung injury through histopathological evaluation. Moreover, we also tested the protein expression of PCNA, P21, Bcl-2 and Bax in the lung. Sildenafil administration rats had a low level of lung injury and inflammation. In addition, sildenafil significantly increased the expression of proliferation-related markers and decreased the expression of apoptosis-related markers in lung tissue. Sildenafil administration may attenuate inflammation and lung injury by promoting proliferation and suppressing apoptosis in SAP rats. [ABSTRACT FROM AUTHOR]