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

炎症介质对脊髓缺血后迟发性截瘫病理生理的影响。

• 批准号: 20791075
• 负责人: YAMASHITA Atsuo
• 金额: $ 2.75万
• 依托单位: Yamaguchi University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Young Scientists (B)
• 财政年份: 2008
• 资助国家: 日本
• 起止时间: 2008 至 2009
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-20791075/
• 关键词: 脳・神経科学; 脊髄; 虚血; 麻酔科学; 脳・神経; 神経科学

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.

最近，与细胞因子相关的高迁移率族蛋白1（HMGB1）成为人们关注的焦点，我们研究了是否可以通过抑制HMGB1的激活来减轻兔子的缺血性脊髓损伤。我们将兔子分为三组（每组n = 5）。 )；对照组，低剂量抗HMGB1抗体组(分段施用1000μg抗HMGB1抗体)，高剂量抗HMGB1抗体组(分段施用1000μg抗HMGB1抗体)； 2000μg抗HMGB1抗体），通过阻断腹主动脉13分钟产生脊髓缺血。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），然后进行7天。计算了脊髓前部正常神经元的数量，神经学评分和缺血性脊髓损伤的正常神经元数量没有显着的组间差异。家兔未还原抑制HMGB1的激活。