Effects and mechanisms of alveolar type II epithelial cell apoptosis in severe pancreatitis-induced acute lung injury

Abstract

This study aimed to examine the role of alveolar type II epithelial cell (AEC II) apoptosis in severe pancreatitis-induced acute lung injury (ALI) and the intervening role of Qingyi decoction (QYT). An SAP model was established in male Sprague-Dawley rats. Immunohistochemical analysis was conducted to observe the pathological changes in the pancreas and lung tissue. AEC II apoptosis was detected by flow cytometry and the free Ca2+ concentration in AECs II was determined by laser scanning confocal microscopy. A radioimmunoassay was performed to determine serum TNF-α content. Quantitative polymerase chain reaction (qPCR) and immunohistochemical analysis were performed to detect the mRNA and protein expression levels of Bax and caspase-8 in the lung tissue. Hematoxylin and eosin staining of lung tissue sections in the severe acute pancreatitis (SAP) group showed pathological changes from control tissue, consistent with acute lung injury (ALI). Flow cytometry showed that the level of AEC II apoptosis in the SAP group was significantly increased compared with that in the control group (P<0.01). Laser scanning confocal microscopy indicated that the free Ca2+ concentration in the AECs II of the SAP group was also significantly increased compared with that in the control (P<0.01). Radioimmunoassay demonstrated that the TNF-α levels were significantly increased in the SAP group compared with those in the control group (P<0.01), and qPCR results showed that the levels of Bax and caspase-8 apoptotic gene expression in the AECs II of the SAP group were significantly elevated (P<0.01). The aforementioned indicators were significantly lower following drug treatment compared with the levels observed in the SAP model group. These results suggest that AEC II apoptosis is involved in the ALI procedure associated with SAP. The mitochondrial pathway and death receptor pathway may have key regulatory roles in AEC II apoptosis. The use of QYT may significantly reduce the extent of lung injury.