Severe
acute pancreatitis (SAP) is initiated by the premature activation of digestive
enzymes within the pancreatic acinar cells, leading to self-digestion and inflammatory responses in pancreatic ductal cells, thus giving rise to
systemic inflammatory response syndrome (SIRS). The most common and serious SIRS is
pancreatitis-associated
lung injury, and inflammatory mediators play an important role in its pathogenesis. Bone marrow-derived mesenchymal stem cells (MSCs) are differentiated into alveolar endothelial cells to replace the damaged alveolar endothelial cells and inhibit inflammatory response in the injured lung tissues. In this study, we aimed to investigate the
therapeutic effect of bone marrow-derived MSCs in rats with
pancreatitis-associated
lung injury. Experimental SAP was induced by a retrograde injection of 5%
sodium taurocholate into the biliopancreatic duct of 75 male Sprague-Dawley rats, which were divided into the SAP group (n=25), the MSC group (n=25) and the
sham-operated group (n=25) to explore the pathology and function of lung tissues and the regulation of inflammatory mediators.
Pulmonary edema was estimated by measuring water content in the lung tissues. Pulmonary
myeloperoxidase (MPO) activity was detected using spectrophotometry. Serum
amylase was detected using the Automatic Biochemistry Analyzer.
Tumor necrosis factor-α (TNF-α) and
substance P (SP)
mRNA levels were determined by quantitative
reverse transcriptase-polymerase chain reaction. Our results showed that serum
amylase activity was significantly decreased in the MSC group compared to the SAP group.
Pulmonary edema was significantly diminished (p<0.05) in the MSC group compared to the SAP group. Typical
acute lung injury was observed in the SAP group, and the pathological changes were mild in the MSC group. The expression of TNF-α and SP
mRNA in lung tissue was diminished in the MSC group compared to the SAP group. In conclusion, MSC
transplantation attenuates
pulmonary edema and
inflammation, and reduces the
mRNA expression of TNF-α and SP in
pancreatitis-associated
lung injury.