中文摘要：

目的 观察外源性酸性成纤维细胞生长因子（aFGF）对大鼠缺血／再灌注（I／R）损伤后肠上皮细胞丝裂素活化蛋白激酶（MAPK）活性的影响，并探讨其与肠上皮细胞增殖能力变化的关系。方法 采用大鼠肠系膜上动脉夹闭法制备缺血45min后再灌注动物模型。132只Wistar大鼠随机分为假手术组、I／R组、aFGF处理组（再灌注即刻颈静脉注射aFGF 4μg）及细胞外信号调节蛋白激酶（ERK1／2）阻断剂PD98059预处理组（缺血前尾静脉注射PD98059 7．5μg，再灌注即刻静脉注射aFGF 4μg）。检测缺血前，I／R15、30min及1、2、6、12和24h时肠上皮细胞增殖能力和MAPK活性。结果 aFGF处理后肠上皮细胞增殖明显增加，同时MAPK活性显著增高。用p44／p42MAPK（ERK1／2）阻断剂PD98059可抑制ERK1／2的活性，使肠上皮细胞增殖减少。结论 aFGF可促进I／R损伤后肠上皮细胞增殖，并可能与其激活肠上皮MAPK有关。

英文摘要：

Objective To investigate the effect of acidic fihrohlast growth factor （aFGF） on p44/p42 mitogen- activated protein kinase （p44/p42 MAPK, extracellular signal regulated protein kinase, ERK1/2） activity in small intestinal epithelium in rat after isehemia/reperfusion （I/R） injury and its relation with the change in small intestinal epithelum in rat after I/R injury as well as the change in proliferation of epithelial cells. Methods Superior mesenteric artery （SMA） was occluded to produce isehemia of the intestine for 45 minutes followed by reperfnsion to reproduce I/R injury. One hundred and thirty -two Wistar rats were randomly divided into sham -operation group, I/R group, aFGF treatment group （4 μg of aFGF was injected into jugular vein after reperfusion）, and PD98059 （antagonist of ERK 1/2） pretreatment group （7.5 btg of PD98059 was injected via tail vein before ischemia and 4 μg of aFGF was injected via jugular vein after reperfusion）. The activity of ERK1/2 and proliferation rate of small intestinal epithelial cells were determined before ischemia and 15 minutes, 30 minutes, 1 hour, 2 hours, 6 hours, 12 hours and 24 hours after reperfusion. Results The activity of ERK1/2 in small intestinal epithelium was higher in aFGF treatment group than in I/R control group, and the proliferation rate in small intestinal epithelial ceils was significantly enhanced in aFGF treatment group. PD98059, the specific inhibitor of ERK1/2, inhibited ERK1/2 activity and reduced the proliferation rate of small intestinal epithelial cells in aFGF treatment group. Conclusion aFGF can promote small intestinal epithelial cell proliferation in I/R injury rats, and this may be related to activition of ERKI/2 in small intestinal epithelium.