Protective effects of remote ischemic preconditioning against spinal cord ischemia-reperfusion injury in rats.

Protective effects of remote ischemic preconditioning against spinal cord ischemia-reperfusion injury in rats.
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DOI:
10.1016/j.jtcvs.2020.03.094
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发表时间:
2020-04
期刊:
The Journal of thoracic and cardiovascular surgery
影响因子:
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通讯作者:
Akira Mukai;K. Suehiro;Aya Kimura;Yohei Fujimoto;T. Funao;Takashi Mori;K. Nishikawa
Akira Mukai;K. Suehiro;Aya Kimura;Yohei Fujimoto;T. Funao;Takashi Mori;K. Nishikawa
中科院分区:
其他
文献类型:
--
作者:
Akira Mukai;K. Suehiro;Aya Kimura;Yohei Fujimoto;T. Funao;Takashi Mori;K. Nishikawa

文献摘要

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目的:通过测定脊髓腹角谷氨酸浓度,探讨远程缺血预适应对脊髓缺血的保护作用及其机制。方法雄性SD大鼠分为5组:假手术组、单纯脊髓缺血组、RIPC/SCI组、MK-801/RIPC/SCI组、MK-801/RIPC/SCI组和MK-801/SCI组,每组6只。在脊髓缺血前80min通过短暂肢体缺血实现远端缺血预适应。MK-801(1 mg/kg,静脉注射)于远程缺血预适应前60分钟静脉注射。微透析法测定脊髓缺血130分钟后腹角谷氨酸浓度。结果脊髓缺血组各时间点谷氨酸浓度均显著高于假手术组(P<0.01)。远端缺血预适应可减轻脊髓缺血引起的谷氨酸升高。当在远程缺血预适应前预先给予MK-801时,脊髓缺血后谷氨酸浓度升高(P<0.01)。免疫荧光显示,远程缺血预适应可抑制运动神经元表面N-甲基-D-天冬氨酸受体2B亚单位的表达(P=0.047)。结论远程缺血预适应可抑制脊髓缺血诱导的前角细胞外谷氨酸水平的升高,并抑制N-甲基-D-天冬氨酸受体2B亚单位的表达。
ObjectivesWe aimed to investigate the protective effect of remote ischemic preconditioning against spinal cord ischemia and find a clue to its mechanism by measuring glutamate concentrations in the spinal ventral horn.MethodsMale Sprague-Dawley rats were divided into 5 groups (n = 6 in each group) as follows: sham; SCI (only spinal cord ischemia); RIPC/SCI (perform remote ischemic preconditioning before spinal cord ischemia); MK-801/RIPC/SCI (administer MK-801, N-methyl-D-aspartate receptor antagonist, before remote ischemic preconditioning); and MK-801/SCI (administer MK-801 without remote ischemic preconditioning). Remote ischemic preconditioning was achieved by brief limb ischemia 80 minutes before spinal cord ischemia. MK-801 (1 mg/kg, intravenous) was administered 60 minutes before remote ischemic preconditioning. The glutamate concentration in the ventral horn was measured by microdialysis for 130 minutes after spinal cord ischemia. Immunofluorescence was also performed to evaluate the expression of N-methyl-D-aspartate receptor 2B subunit in the ventral horn 130 minutes after spinal cord ischemia.ResultsThe glutamate concentrations in the spinal cord ischemia group were significantly higher than in the sham group at all time points (P < .01). Remote ischemic preconditioning attenuated the spinal cord ischemia–induced glutamate increase. When MK-801 was preadministered before remote ischemic preconditioning, glutamate concentration was increased after spinal cord ischemia (P < .01). Immunofluorescence showed that remote ischemic preconditioning prevented the increase in the expression of N-methyl-D-aspartate receptor 2B subunit on the surface of motor neurons (P = .047).ConclusionsOur results showed that remote ischemic preconditioning prevented spinal cord ischemia–induced extracellular glutamate increase in ventral horn and suppressed N-methyl-D-aspartate receptor 2B subunit expression.