中文摘要：

目的 观察小鼠小肠缺血再灌注损伤（IRI）模型中缺血预适应（IPC）对小肠IRI的保护作用,并检测c-Fos和c-Jun的变化,探讨其小肠IRI和IPC中的作用机制.方法 建立雄性C57BL/6小鼠小肠IRI模型,分为Sham组（假手术）、IRI组（单纯IRI）和IPC组（IPC＋IRI）3组.采集3组术后再灌注0、30、60、90、120min小肠组织,实时定量反转录聚合酶链反应（RT-qPCR）检测不同时间点c-Fos和c-Jun的mRNA表达;免疫组织化学检测不同时间点小肠组织的c-Fos、c-Jun、增殖细胞核抗原（PCNA）蛋白表达;原位缺口末端标记法（TUNEL）法检测不同时间点小肠上皮细胞凋亡情况.结果 RT-qPCR检测结果显示与对照组比较,IRI组小肠组织中c-Fos和c-Jun mRNA表达强度不断上升,分别于再灌注30min和60min时达峰值（12.34±2.95、11.65±2.43）,并且明显高于IPC组（P=0.011、P=0.017）.免疫组织化学检测显示IRI组再灌注30-60min时c-Fos（189.62±47.45、174.31±32.57）（P=0.026、P=0.029）和60-120min（71.31±11.54、97.46±14.48）（P=0.031、P=0.027）时c-Jun表达明显高于IPC组.IRI组PCNA表达不断增强,60min达峰值（392.74±67.04）后下降,并且明显高于IPC组（P=0.013）;TUNEL染色显示与对照组比较随再灌注时间延长,IRI组和IPC组的凋亡指数（AI）均高于对照组,但IPC组再灌注90-120min的AI值明显低于IRI组（P=0.036、P=0.028）.结论 IPC对小鼠小肠IRI具有显著的保护作用,c-Fos和c-Jun可能是介导小鼠小肠IPC保护作用的重要内源性活性介质.

英文摘要：

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.