Preconditioning Effects On Expression Of C-fos And C-jun In The Mouse Small Intestinal Epithelium After Ischemia-reperfusion Injury

Backgroup and Objective:Ischemia-reperfusion injury (IRI) of the intestine is a significant problem which influence the short-term and long-term graft survival in small bowel transplant patients. Although the ischemic preconditioning (IPC) has been considered as a potential strategy to overcome IRI, the effects and exact mechanism of IPC confers protection in the intestine is unclear. Recently, there is some evidence that proliferation and apoptosis in the postischemic intestinal epithelial cells (IECs) are closely related to the expression patterns of c-fos and c-jun. The purpose of this study is to investigate the effects of IPC on expression of c-fos and c-jun following intestianl IRI and its roles in cellular regeneration and apoptosis.Method:Intestinal ischemia was induced by occluding the superior mesenteric artery with a clamp, C57BL/6 male mice were randomly divided into IR group, intestianl IPC group and sham group (n=15 for each group). The mice were subjected to 25-minute intestinal ischemia and preceded by 10-minute preconditioning. The intestinal tissue in each group were collected to detect the sequential expression of c-fos and c-jun using RT-PCR and immunohistochemical staining after 0-, 30-, 60-, 90-,120-minute reperfusion. The proliferation and apoptosis of IECs were detected by immunohistochemistry of PCNA expression and the in situ TUNEL method, respectively.Results:The mRNA levels of c-fos and c-jun were reduced at different time points in IPC group compared with IR group(P<0.05). The PCNA immunoreactivity in IR group seemed stronger than the IPC group from 30 to 60 minutes after reperfusion(P<0.05), and the apoptosis of IR group higher than IPC group at 90 to 120 minutes after reperfusion(P<0.05).Conclusion:Our results show that IPC can protects IECs from IRI in the mouse intestinal IRI model, and the c-fos and c-jun may involve in this beneficial effects. Although their underlying regulatory pathway and biological roles remain unclear, it may be a new target to prevent intestinal damage after suffering from IRI.