西维来司钠对大鼠脊髓缺血再灌注损伤后NF-κBp65和HMGB1表达的影响

摘要

Objective To study the expression variation and significance of NF-κBp65, HMGB1 in rats after spinal cord ischemia-reperfusion injury and the impact of Sivelestat sodium on this expression. Methods First of all, blocked around the abdominal aorta between the renal artery of rats for 30 minutes by surgical methods. Next , restore the blood supply. Establishment of a rat model of spinal cord ischemia-reperfusion. 65 SD rats were randomly assigned into the control group (NC), sham group (SH), ischemia-reperfusion group (IR) and Ischemia-reperfusion + Sivelestat sodium group (SS). Used Western blotting and RT-PCR methods to detect the expression of NF-κBp65, HMGB1 in each group at each time point in spinal cord tissues. Results WB and RT-PCR results showed that NF-κBp65 and HMGB1 expression levels had no signifi-cant difference in SH group compared with the NC group at each time point (3h, 12h, 24h, 72h), P＞0.05. NF-κBp65 and HMGB1 expressions were significantly higher in the IR group at each time point (P＜0.05). Reached the peak after 24 hours and then declined showly. NF-κBp65 and HMGB1 in SS group were lower than the corresponding time points in IR group (P＜0.05), but still higher than the SH group. Conclusion Sodium sivelestat can protect the spinal cord ischemia-reperfusion injury , restraining the radioactivation of NF-κBp65 and HMGB1, lessening the expression of NF-κBp65 and HMGB1 may be associat-ed with it.%目的 研究NF-κBp65和HMGB1在脊髓缺血再灌注损伤(spinal cord ischemic reperfusion injury,SCII)后的表达及西维来司钠(Sivelestat sodium)对这种表达的影响.方法 通过外科手术方法,使用无创动脉夹夹闭大鼠左右肾动脉之间的腹主动脉30min,然后松开动脉夹,恢复血供,建立SCII大鼠模型. 取65只SD大鼠,随机分成空白对照组(NC)、假手术组(SH)、缺血再灌注组(IR)和西维来司钠治疗组(SS). SH组、IR组、SS组再按照3h、12h、24h、72h 4个时间点分为4个亚组. 运用免疫印迹法(Westem blotting,WB)和RT-PCR法分别检测以上各组各时间点脊髓组织中NF-κBp65和HMGB1的表达及变化.结果 WB及RT-PCR结果显示,与NC组相比,SH组各时间点(3h、12h、24h、72h)NF-κBp65和HMGB1的表达水平差异无统计学意义(P＞0.05);IR组各时间点 NF-κBp65和HMGB1的表达显著增高(P＜0.05),且在24h到达高峰,而后缓慢下降. SS组中NF-κBp65和HMGB1的表达较IR组对应时间点相对降低(P＜0.05),但表达依然比SH组高. 结论西维来司钠对SCII有一定的保护作用,其机制可能与抑制NF-κBp65和HMGB1的活化、降低NF-κBp65和HMGB1的表达有关.