The influence of inflammatory mediators on the pathophysiology of delayed paraplegia after spinal cord ischemia.

近年来，与细胞因子相关的高迁移率族蛋白1（HMGB1）成为研究热点。我们研究了是否减少缺血性脊髓损伤的兔抑制HMGB1的激活。将家兔分为3组（每组n=5）：对照组、低剂量抗HMGB1抗体组（节段性给予1000μg抗HMGB1抗体）、高剂量抗HMGB1抗体组（节段性给予2000μg抗HMGB1抗体）。通过阻断腹主动脉13 min造成脊髓缺血。再灌注后，每天评估后肢运动功能（评分范围：4，正常至0，截瘫），持续7 d，然后计数脊髓前部正常神经元的数量。神经功能评分和正常神经元数量无显著组间差异。抑制HMGB1的活化并不能减轻兔脊髓缺血损伤。

Recently, high mobility group box 1 protein (HMGB1) related to cytokine gets into the limelight. We investigated whether the ischemic spinal cord injury in rabbits was reduced to inhibit the activation of HMGB1. We assigned rabbits to three groups (n=5 in each); a control group, low dose anti- HMGB1 antibody group (segmental administration of 1000μg anti- HMGB1 antibody), high dose anti- HMGB1 antibody group (segmental administration of 2000μg anti- HMGB1 antibody). Spinal cord ischemia was produced by occluding the abdominal aorta for 13 min. After the reperfusion, hindlimb motor function (score range: 4, normal to 0, paraplegia) was assessed daily for 7 days, and then the number of normal neurons in the anterior spinal cord was counted. There were no significant intergroup differences in neurological scores and the numbers of normal neurons. The ischemic spinal cord injury in rabbits was not reduced to inhibit the activation of HMGB1.