FGFR3与小鼠小肠缺血再灌注损伤后肠上皮细胞凋亡的关系  

Relationship between FGFR3 and Epithelium Apoptosis after Intestinal Mucosal Ischemia-reperfusion Injury in Mice

作　　者：朱渝军[1] 黄显凯[1] 

机构地区：[1]第三军医大学大坪医院野战外科研究所全军战创伤中心,重庆400042

出　　处：《华南国防医学杂志》2009年第3期9-11,18,共4页Military Medical Journal of South China

基　　金：重庆市自然科学基金项目(CSTC-2006BB5056)

摘　　要：目的探讨成纤维细胞因子受体3(fibroblast growth factor receptor 3,FGFR3)与小鼠小肠粘膜缺血再灌注损伤后肠上皮细胞凋亡的关系。方法应用小肠缺血再灌注模型,检测野生小鼠及FGFR3增强小鼠小肠缺血再灌注损伤后1、3、6 h和1、3天各时间点肠粘膜结构、粘膜隐窝上皮细胞增殖能力及粘膜上皮细胞凋亡的改变。结果肠缺血再灌注l、3、6 h,肠粘膜损害明显,粘膜上皮细胞凋亡增加,粘膜隐窝上皮细胞增殖增多;肠粘膜再生1、3天组肠粘膜上皮细胞凋亡明显减少,粘膜隐窝上皮细胞增殖活性逐渐降低,肠粘膜结构恢复至正常。FGFR3增强小鼠在各时间点增殖能力明显强于野生小鼠,凋亡程度及肠粘膜损害程度均轻于野生小鼠。结论FGFR3抑制肠上皮细胞凋亡,促进增殖,可能在肠缺血再灌注损伤及肠再生修复过程中起重要作用。Objective To investigate the relationship between fibroblast growth factor receptor 3 （FGFR3） and the apoptosis of epithelial cells after intestinal mucosal ischemia-reperfusion injury in mice. Methods A.n experimental model of intestinal ischemia-reperfusion in mice was established. Intestinal mucosal morphology, apoptosis and proliferation activities of intestinal epithelial cells were observed for wild mice （wild I/R group） and FGFR3-enhaneed mice （GFR3 ^＋ I/R group） 1, 3, 6 hours and 1,3 days after reperfusion. Results Progressively severe mueosal injury, dramatically increased epithelial apoptosis and epithelial proliferation were observed 1, 3, 6 hours after reperfusion. The recovery of mucosal injury and attenuation of epithelial apoptosis were observed 1, 3 days after reperfusion. Proliferation activity gradually de creased. The damage and apoptosis in small intestinal epithelium were significantly lower, and proliferation ability was significantly higher in FGFR3^ ＋ I/R group than wild I/R group. Conclusion FGFR3 can attenuate the apoptosis of.intestinal epithelium and improve the proliferation. FGFR3 plays an important role in intestinal mucosal ischemia-reperfusion damage and repair.

关 键 词：成纤维细胞因子受体3 缺血再灌注损伤 细胞凋亡 

分 类 号：R363.14[医药卫生—病理学]