兔脊髓缺血再灌注损伤后能量代谢与NF-κBp65表达变化

摘要

目的：探讨脊髓缺血再灌注损伤（SCIRI）中能量代谢与NF-κBp65的变化规律。方法：40只新西兰大白兔采用肾下腹主动脉阻断45 min，建立脊髓缺血再灌注损伤模型。分别于缺血前、缺血45 min及再灌注30、60、120 min时取脊髓测定腺苷酸（ADP、AMP、ATP）、活性氧（ROS）、核转录因子-κBp65（NF-κBp65）、抑制蛋白-κBα（I-κBα）和细胞间黏附分子-1（ICAM-1）蛋白表达变化。结果：与缺血前比较，缺血45 min及再灌注30、60、120 min时脊髓腺苷酸及I-κBα均降低（P<0.01），ROS、NF-κBp65和ICAM-1均升高（P<0.01）。结论：SCIRI中ICAM-1和NF-κBp65表达上调加重脊髓能量代谢障碍。%Objective:To assess the changes of energy metabolism and NF-κBp65 during spinal cord ischemia and reperfusion injury(SCIRI). Method:The SCIRI model was made by clamping the infrarenal aortic for 45 minutes in 40 rabbits.Reactive oxygen species(ROS),the expression of nuclear factor-kappa Bp65(NF-κBp65),inhibitor-Kappa Bα(I-κBα),intercellular adhesion molecule(ICAM-1)and the content of adenine nucleotide(ADP,AMP and ATP)in spinal cord tissue were determined before ischemia,45 minutes after ischemia,30,60 minutes and 120 minutes after reperfusion. Result:The spinal cord content of adenine nucleotide and I-κBαdecreased while ROS,the expressions of NF-κBp65and ICAM-1 increased at 45 minutes after ischemia,30,60 minutes and 120 minutes after reperfusion as compared to the value before ischemia(P<0.01). Conclusion:The upregulation of the expression of ICAM-1 and NF-κBp65 aggravates the energy metabolism disorder of spinal cord during SCIRI.