Follistatin-like 1 ameliorates severe acute pancreatitis associated lung injury via inhibiting the activation of NLRP3 inflammasome and NF-κB pathway

This study helps us understand the mechanism of FSTL-1 in SAPALI and might provide a potential new strategy for the treatment of SAPALI.

SAP model was induced by intraperitoneal injection of the L-arginine in C57BL/6 mice. The haematoxylin and eosin (H&E) staining was applied to determine the severity of lung and pancreatic injury. ELISA kits were used to determine serum amylase and inflammatory cytokines levels. TUNEL staining was carried out to measure cell apoptosis. Western blotting was applied to analyze the related proteins of NLRP3 inflammasome and NF-κB pathways.

Severe acute pancreatitis (SAP) is one of the most common abdominal conditions of digestive system that usually causes acute lung injury through systemic inflammation. Follistatin-like 1 (FSTL-1) has been reported to have anti-inflammatory and anti-apoptotic effects in a variety of diseases. The aim of this study was to investigate the effects of FSTL-1 on SAP-associated lung injury (SAPALI) and the underlying mechanism.

FSTL-1 was significantly increased in the lung of SAP mice. Knockout of FSTL-1 ameliorated pancreatic injury, lung injury, inflammation and apoptosis in mice with SAP. Moreover, the protein levels of NLRP3, ASC, Caspase-1, p-p65 and p-IκBα were obviously reduced in the FSTL-1 KO+SAP group in comparison with SAP group, suggesting that inhibition of FSTL-1 repressed the activation of the NLRP3 inflammasome and NF-κB pathway.