Abstract
Objective To investigate the effects of ischemia postconditioning (IPC) on the expression of c-Fos and c-Jun following intestianl ischemia-reperfusion injury (IRI) and its roles in cellular regeneration and apoptosis. Methods 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-min intestinal ischemia and preceded by 10-min preconditioning. The intestinal tissues in each group were collected for detection of the sequential expression of c-Fos and c-Jun using real-time quantitative reverse transcriptase-polymerase chain reaction (RT-qPCR) and c-Fos, c-Jun and proliferating cell nuclear antigen (PCNA) using immunohistochemical staining after 0-, 30-, 60-, 90-, 120-min reperfusion. The apoptosis of IECs was examined by the in situ TdT-mediated dUTP nick end labeling (TUNEL) method. Results The mRNA levels of c-Fos and c-Jun were reduced at different time points in IPC group as compared with IR group and peaked at 30 min and 60 min (12.34±2.95 and 11.65±2.43) (P=0.011, P=0.017). The PCNA immunoreactivity in IR group was stronger than in IPC group from 30 to 60 min after reperfusion and peaked at 60 min (392.74±67.04) (P=0.013), and the apoptosis rate in IR group was higher than in IPC group at 90 to 120 min after reperfusion(P=0.036, P=0.028). Conclusion IPC can protect IECs from IRI in the mouse intestinal IRI model, and the c-Fos and c-Jun may involve in this beneficial effects. Key words: Intestinal ischemia-reperfusion injury; Ischemic preconditioning; Activatorprotein-1; c-Fos; c-Jun
Published Version
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