中文摘要：

目的 探讨促红细胞生成素（EPO）对大鼠肠缺血再灌注损伤（IRI）的作用及其机制.方法 随机将30只雄性SD大鼠分成假手术组（Sham组）、缺血再灌注损伤组（IRI组）和EPO预处理组（EPO组）.EPO组在手术前0.5h给予EPO腹腔注射（5000U/kg）,Sham组和IRI组在手术前30min给予等量生理盐水腹腔注射.手术分离肠系膜上动脉,通过夹闭30min、再灌注60 min 诱导缺血再灌注损伤.HE染色观察肠道黏膜病理学形态学变化,PCR检测白细胞介素6（IL-6）和干扰素（inteferon gamma,IFN-γ）和肿瘤坏死因子（TNF-α）.Western blotting（WB） 检测JAK2,STAT3,p-JAK2和 p-STAT3.结果 与Sham组相比,IRI组肠黏膜损伤明显增加.PCR显示IL-6、IFN-γ和TNF-α也明显上调,WB显示表达p-JAK2,p-STAT3明显增加,但JAK2和STAT3无明显变化.与IRI组相比,EPO组小肠黏膜损伤明显减少,IL-6、IFN-γ和TNF-α表达降低,p-JAK2和p-STAT3表达进一步增加,但JAK2和STAT3无明显变化.结论 EPO预处理可通过激活JAK2/STAT3信号通路抑制炎症反应,从而减轻肠缺血再灌注损伤.

英文摘要：

Objective To investigate the potential protection of erythropoietin（EPO） on intestinal isehemia - reperfusion injury （IRI） and its mechanism. Methods Thirty Sprague-Dawley rats were ran- domly divided into 3 groups ： sham operation group （ sham ） , IRI group and IR plus EPO preconditioning group. EPO was administered by intraperitoneal injection （ i. p. , 5000 U/kg） 30 rain prior to operation in EPO group, and equal volume of saline was administered in the other 2 groups. The intestinal IRI was induced in IRI group and IR ＋ EPO group using bulldog clamps on superior mesenteric artery with 30 rain of ischemia followed by 60 min of reperfusion. The pathology of intestinal tissues was observed by HE stai- ning. The mRNA levels of IL-6, TNF-α and IFN-γ were measured by PCR. The expression of JAK2, STAT3 ,p-JAK2 and p-STAT3 was measured by Western blotting. Results Compared with the sham group, the level of mesenteric injuries in IRI group was significantly higher. Moreover, the mRNA levels of IL-6, TNF-α and IFN-γ and the protein expression levels of p-JAK2 and p-STAT3 were all higher than the sham group, but the protein expression level of JAK2 and STAT3 had no significant difference. Compared to the IRI group, the level of mesenteric injuries, and the mRNA levels of IL-6, TNF-α and IFN-γ in the EPO group were significantly attenuated, the expression of p-JAK2 and p-STAT3 were further increased, and the protein expression levels of JAK2 and STAT3 had no significant difference. Conclusion EPO preconditioning can protect against intestinal IRI in rats by activating JAK2/STAT3 signal pathway to attenuate inflammation.