Timing of xenon-induced delayed postconditioning to protect against spinal cord ischaemia-reperfusion injury in rats.

Timing of xenon-induced delayed postconditioning to protect against spinal cord ischaemia-reperfusion injury in rats.
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氙诱导的延迟后处理的时机以防止大鼠脊髓缺血再灌注损伤。

DOI:
10.1093/bja/aet352
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发表时间:
2014-07
影响因子:
9.8
通讯作者:
Gao, Z F
Gao, Z F
中科院分区:
医学1区
文献类型:
--
作者:
Yang, Y W;Cheng, W P;Lu, J K;Dong, X H;Wang, C B;Zhang, J;Zhao, L Y;Gao, Z F

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背景 本研究旨在评估氙诱导的延迟后处理对脊髓缺血再灌注损伤(IRI)的神经保护作用,并确定在脊髓IRI大鼠模型中最佳神经保护的给药时间。 方法 将50只雄性大鼠随机分为假手术组、对照组和3个氙后处理组(n=10/组)。对照组行脊髓IRI,再灌注开始时立即吸入50%氮气/50%氧气3 h。三个氙后处理组进行相同的手术程序,并立即吸入50%氙/50%氧3小时,在再灌注开始或1和2小时后再灌注。假手术组不阻断主动脉,吸入50%氮气/50%氧气。在再灌注4、24和48 h采用Basso、Beattie和Bresnahan评分评估神经功能。组织学检查采用尼氏染色和免疫组化,细胞凋亡检测采用末端脱氧核苷酸转移酶介导的脱氧尿苷三磷酸缺口末端标记染色。 结果 与对照组相比,三个氙后处理组的神经功能的结果显示出改善,并有更多的形态正常的神经元在48小时的再灌注。与对照组相比,氙处理大鼠的凋亡细胞死亡减少,Bcl-2/Bax免疫反应性的比率增加。 结论 氙后处理2小时后再灌注提供保护对脊髓IRI大鼠,但最大的神经保护发生在再灌注1小时的氙。
BACKGROUND This study was designed to assess the neuroprotective effect of xenon-induced delayed postconditioning on spinal cord ischaemia-reperfusion injury (IRI) and to determine the time of administration for best neuroprotection in a rat model of spinal cord IRI. METHODS Fifty male rats were randomly divided equally into a sham group, control group, and three xenon postconditioning groups (n=10 per group). The control group underwent spinal cord IRI and immediately inhaled 50% nitrogen/50% oxygen for 3 h at the initiation of reperfusion. The three xenon postconditioning groups underwent the same surgical procedure and immediately inhaled 50% xenon/50% oxygen for 3 h at the initiation of reperfusion or 1 and 2 h after reperfusion. The sham operation group underwent the same surgical procedure without aortic occlusion, and inhaled 50% nitrogen/50% oxygen. Neurological function was assessed using the Basso, Beattie, and Bresnahan score at 4, 24, and 48 h of reperfusion. Histological examination was performed using Nissl staining and immunohistochemistry, and apoptosis was detected by terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labelling staining. RESULTS Compared with the control group, the three xenon postconditioning groups showed improvements in neurological outcomes, and had more morphologically normal neurones at 48 h of reperfusion. Apoptotic cell death was reduced and the ratio of Bcl-2/Bax immunoreactivity increased in xenon-treated rats compared with controls. CONCLUSIONS Xenon postconditioning up to 2 h after reperfusion provided protection against spinal cord IRI in rats, but the greatest neuroprotection occurred with administration of xenon for 1 h at reperfusion.
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