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目的 研究失血性休克及复苏后解偶联蛋白 2 (UCP2 )在肠上皮线粒体功能损伤中的作用。方法 复制大鼠失血性休克复苏模型 ,分别于休克前、休克 90分钟及复苏 2小时、6小时、12小时、2 4小时取小肠上皮 ,用Western blot法测线粒体UCP2的含量 ,用荧光分光光度法测UCP2对线粒体膜电位 (MP)、线粒体内活性氧 (ROS)产生的影响作用 ,用高效液相色谱法 (HPLC)测组织中三磷酸腺苷 (ATP)的含量。结果 (1)失血性休克及复苏后肠上皮线粒体中UCP2含量增高 (P <0 .0 5 ) ;(2 )UCP2可降低MP并抑制线粒体内ROS产生 ,但UCP2对线粒体内ROS产生的调节作用受MP影响 ;(3)失血性休克后 ,肠上皮组织中ATP含量明显下降 ,是对照组的 2 0 .81% ,复苏后 2 4小时 ,其水平仍低于正常。结论 UCP2可能参与失血性休克及复苏后肠上皮线粒体功能的损伤
Objective To investigate the role of uncoupling protein 2 (UCP2) in functional damage of intestinal epithelial mitochondria after hemorrhagic shock and resuscitation. Methods The hemorrhagic shock model of rats was reproduced and the intestine of small intestine was taken before shock, 90 minutes after shock and 2 hours, 6 hours, 12 hours and 24 hours after resuscitation respectively. The content of mitochondrial UCP2 was determined by Western blot and the fluorescence spectrophotometry The effect of UCP2 on mitochondrial membrane potential (MP) and reactive oxygen species (ROS) in mitochondria was measured by spectrophotometry. The content of adenosine triphosphate (ATP) in tissues was determined by high performance liquid chromatography (HPLC) Results (1) The content of UCP2 in intestinal epithelial mitochondria increased after hemorrhagic shock and resuscitation (P <0.05). (2) UCP2 could reduce MP and inhibit the production of ROS in mitochondria, but the regulation of UCP2 on mitochondrial ROS generation Affected by MP; (3) After hemorrhagic shock, ATP content in intestinal epithelial tissue decreased significantly, 20.81% of the control group, 24 hours after resuscitation, the level is still lower than normal. Conclusion UCP2 may be involved in mitochondrial function damage after hemorrhagic shock and resuscitation