中文摘要：

背景：酸性成纤维细胞生长因子可以促进多种创面愈合，往内脏损伤修复中起雨要促进作用。目的：观察外源性酸性成纤维细胞生长因子干预肠缺血再灌注损伤大鼠后p38MAPK和成纤维细胞qi长凶子受体2的表达。方法：以大鼠肠系膜上动脉灾闭45min造成肠缺血再灌注损伤模型，于再灌注即刻心用改构体酸性成纤维细胞生长因子进行干预。分别于再灌注2，6，12，24h取大鼠小肠纰织标本，川于实验。结果与结论：在正常大鼠，成纤维细胞生长因子受体2主要分们在小肠绒毛t皮细胞的肠腔侧、侧避和小肠隐窝朝向隐窝腔的一侧细胞膜上。缺血一再灌注初期，p38MAPK蚩白及成纤维细胞生三长因子受体2蛋自和mRNA的表达朱发生明显变化，随着再灌注时间的延氏其逐渐增强．并于再灌注后6-12h达高峰。经酸性成纤维细胞生长㈧子治疗后，大鼠小肠组织p38MAPK蛋白及成纤维细胞生长因子受体2蛋白和mRNA的表达进一步增强，小肠黏膜损伤程度减轻。说明酸性成纤维细胞生长因子可通过上调成纤维细胞生长园子受体2和p38MAPK的表达促进肠缺血再灌注损伤的修复。

英文摘要：

BACKGROUND： Different types of wound healing can be promoted by acidic fibroblast growth factors. It plays an important role in the repair of visceral injury. OBJECTIVE： To explore the effect of exogenous acidic fibroblast growth factor on the expression of p38MAPK and fibroblast growth-factor receptor 2 in rats with intestinal ischemia-reperfusion injury. METHODS： Rat superior mesenteric artery was microsurgical clipping for 45 minutes to construct intestinal ischemia＊reperfusion injury model. Rats were treated with modified acidic fibroblast growth factor immediately after reperfusion. Rat small intestines samples were collected at the 2nd, 6th, 12th and 24th hours after reperfusion to examine. RESULTS AND CONCLUSION： Fibroblast growth-factor receptors 2 were mainly distributed in epithelial cells of small intestinal villi at intestinal cavity, side wall and on the cell membrane of crypts toward cavity. There was no significant change in the expression of fibroblast growth-factor receptor 2 and p38MAPK in protein and mRNA level at the primary stage after reperfusion. Then the expression of fibroblast growth-factor receptor 2 and p38MAPK increased gradually along with the extension of time, and peaked at the 6th to 12th hours after reperfusion. The protein and mRNA expression of fibroblast growth-factor receptor 2 and p38MAPK in rat small intestines was further enhanced after treated with acidic fibroblast growth factor. These findings demonstrate that acidic fibroblast growth factor can promote the repair of intestinal ischemia-reperfusion injury by up-regulating the expression of fibroblast growth-factor receptor 2 and p38MAPK.