Background: Resistin-like molecule-α (RELMα) has diverse
regulatory functions in inflammation, but its role in severe acute pancreatitis
(SAP) and acute pancreatitis associated lung injury (APALI) remains
Methods: SAP was induced in rats. RELMα protein expression was detected
in lung tissue of rats to determine the relationship between APALI and
RELMα. To investigate the effect of RELMα overexpression or knockdown
on APALI, rats were given an intravenous injection of adenovirus vector
before SAP induction. Lung and pancreatic samples were harvested 16 h
after induction. After detection of RELMα protein levels, the severity of
pancreatic and pulmonary injury was scored histologically, and serum and tissue levels of
inflammatory mediators were measured. TUNEL assay and immunofluorescence were used
to estimate pulmonary apoptosis and endothelial barrier integrity in lung tissue of SAP rats
with RELMα knockdown.
Results: RELMα expression was significantly up-regulated in APALI and was related to the
lung injury index. RELMα overexpression aggravated the release of inflammatory cytokines
including interleukin (IL)-1β, IL-6, IL-8, tumor necrosis factor-α, and serum C-reaction protein;
the expression of inflammatory mediators phosphorylated (p)-AKT, p-P65, p-P38 mitogen
activated protein kinase, p-extracellular regulated kinase, and intracellular adhesion
molecule-1; and lung injury. RELMα knockdown had opposite effects. In addition, RELMα
knockdown improved expression of proliferative cellular nuclear antigen, Bcl-2, zonal
occluding-1 and Claudin-1 in lung tissue of SAP rats.
Conclusion: RELMα is associated with lung injury severity in SAP. RELMα augments
inflammatory activity by increasing inflammatory cytokine release.