《中国康复理论与实践》 ›› 2003, Vol. 9 ›› Issue (08): 477-479.

• 基础研究 • 上一篇    下一篇

白细胞介素11预防大鼠肠道缺血性损伤的机制探讨

刘静波1,2;张泰昌3   

  1. 1.首都医科大学康复医学院 北京市 100068;2.北京博爱医院内科 北京市 100068;3.首都医科大学附属北京宣武医院消化内科 北京市 100053
  • 收稿日期:2003-06-04 出版日期:2003-08-25 发布日期:2003-08-25

Potential protective mechanism of rhIL-11 pretreatment on intestinal ischemia/reperfusion injury of rats

LIU Jing-bo, ZHANG Tai-chang   

  1. Department of Internal Medicine, Beijing Charity Hospital, Beijing 100068, China
  • Received:2003-06-04 Published:2003-08-25 Online:2003-08-25

摘要: 目的探讨重组人白细胞介素11(recombinant human interleukin-11,rhIL-11)预处理对大鼠肠道缺血再灌注损伤保护作用的分子机制。方法夹闭大鼠肠系膜上动脉1h后松夹建立缺血再灌注模型。将56只雄性Wistar大鼠随机分为正常对照组(A)、单纯缺血再灌注组(B)、生理盐水对照组?和rhIL-11预处理组(D)。C组和D组分别于夹闭前 2天给予生理盐水 (0.25ml/只/d)或rhIL-11(600μg/kg/d)。于再灌注6h和24h时分别处死各组大鼠,以凋亡细胞原位末端标记技术(TdT mediatedd UTPnickendlabeling,TUNEL)检测组织中细胞凋亡情况,用免疫组织化学法检测抗凋亡因子bcl-2及蛋白激酶casPase 3和casPase 8的表达水平。同时以苏木素 伊红 (hematoxylin eosin,HE)染色观察形态学病理改变。 结果HE及TUNEL检测显示,rhIL-11预处理组大鼠肠屏障功能的损伤程度较B、C组显著减轻,凋亡细胞数量减少,casPase 3和casPase 8的表达水平也低于B、C组,而bcl-2的表达量增加。结论rhIL-11预处理对大鼠缺血再灌注损伤的保护作用可能与抑制casPase 3和casPase 8的表达,激活bcl-2的表达有关。

关键词: 重组人白细胞介素11, 缺血再灌注损伤, 肠道, 蛋白激酶

Abstract: ObjectiveTo explore the molecular mechanism of protective effects of recombinant human interleukin-11( rhIL-11) pretreatment on intestinal ischemia/reperfusion (I/R) injury of rats.MethodsThe I/R model of rat was produced by clampi ng the superior mesenteric artery for 1 hour, animals were divided randomly into the normal control group (A), I/R group (B), normal saline control group? and rhIL-11 pretreatment group (D). In group C and D, animals were administered w ith saline(0.25ml/rat/day)or rhIL-11 (600μg/kg/day) two days before the oper ation. Rats in different groups were sacrificed at 6 hours and 24 hours after re perfusion respectively. Intestinal apoptosis was detected by TUNEL staining, and the expression of bcl-2, caspase 3 and caspase 8 were determined by immunohist ochemistry. Meanwhile pathologic pictures were detected by hematoxylin-eosin (HE) staining.ResultsHE and TUNEL examinations showe d that in group D, the intestinal barrier was damaged obviously slighter than th at in the group B and group C, with decreased apoptosis cells, meanwhile, expres sion levels of caspase 3 and caspase 8 were lower, and bcl-2 was higher than th e group B and group C.Conclusions The protective e ffect of rhIL-11 pretreatment on rat intestinal I/R injury might be caused by t hat the expression of activities of caspase 3 and caspase 8 are inhibited and b cl-2 is activated.

Key words: recombinant human interleukin- 11 (rhIL-11), ischemia/reperfusion injury, intestine, protein kinase