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电针预处理通过以脂氧素A受体依赖性方式抑制高迁移率族蛋白B1的产生来减轻脊髓缺血再灌注损伤。

Electroacupuncture pretreatment attenuates spinal cord ischemia-reperfusion injury via inhibition of high-mobility group box 1 production in a LXA receptor-dependent manner.

作者信息

Zhu Xiao-Ling, Chen Xin, Wang Wei, Li Xu, Huo Jia, Wang Yu, Min Yu-Yuan, Su Bin-Xiao, Pei Jian-Ming

机构信息

Department of Physiology, Fourth Military Medical University, Xi'an 710032, China; Department of Anesthesiology, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China.

Department of Anesthesiology, Shaanxi Provincial People's Hospital, Xi'an 710068, China.

出版信息

Brain Res. 2017 Mar 15;1659:113-120. doi: 10.1016/j.brainres.2017.01.008. Epub 2017 Jan 12.

DOI:10.1016/j.brainres.2017.01.008
PMID:28089662
Abstract

Paraplegia caused by spinal cord ischemia is a severe complication following surgeries in the thoracic aneurysm. HMGB1 has been recognized as a key mediator in spinal inflammatory response after spinal cord injury. Electroacupuncture (EA) pretreatment could provide neuroprotection against cerebral ischemic injury through inhibition of HMGB1 release. Therefore, the present study aims to test the hypothesis that EA pretreatment protects against spinal cord ischemia-reperfusion (I/R) injury via inhibition of HMGB1 release. Animals were pre-treated with EA stimulations 30min daily for 4 successive days, followed by 20-min spinal cord ischemia induced by using a balloon catheter placed into the aorta. We found that spinal I/R significantly increased mRNA and cytosolic protein levels of HMGB1 after reperfusion in the spinal cord. The EA-pretreated animals displayed better motor performance after reperfusion along with the decrease of apoptosis, HMGB1, TNF-α and IL-1β expressions in the spinal cord, whereas these effects by EA pretreatment was reversed by rHMGB1 administration. Furthermore, EA pretreatment attenuated the down-regulation of LXA receptor (ALX) expression induced by I/R injury, while the decrease of HMGB1 release in EA-pretreated rats was reversed by the combined BOC-2 (an inhibitor of LXA receptor) treatment. In conclusion, EA pretreatment may promote spinal I/R injury through the inhibition of HMGB1 release in a LXA receptor-dependent manner. Our data may represent a new therapeutic technique for treating spinal cord ischemia-reperfusion injury.

摘要

脊髓缺血所致截瘫是胸主动脉瘤手术后的一种严重并发症。HMGB1已被公认为脊髓损伤后脊髓炎症反应的关键介质。电针预处理可通过抑制HMGB1释放对脑缺血损伤起到神经保护作用。因此,本研究旨在验证电针预处理通过抑制HMGB1释放来预防脊髓缺血再灌注(I/R)损伤这一假说。对动物连续4天每天进行30分钟的电针刺激预处理,随后通过将球囊导管置入主动脉诱导20分钟的脊髓缺血。我们发现脊髓再灌注后脊髓I/R显著增加了HMGB1的mRNA和胞质蛋白水平。电针预处理的动物再灌注后运动功能表现更佳,同时脊髓中凋亡、HMGB1、TNF-α和IL-1β的表达降低,而给予rHMGB1可逆转电针预处理的这些作用。此外,电针预处理减轻了I/R损伤诱导的LXA受体(ALX)表达下调,而联合使用BOC-2(一种LXA受体抑制剂)处理可逆转电针预处理大鼠中HMGB1释放的减少。总之,电针预处理可能通过以LXA受体依赖的方式抑制HMGB1释放来减轻脊髓I/R损伤。我们的数据可能代表了一种治疗脊髓缺血再灌注损伤的新治疗技术。

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