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脂氧素A4改善兔模型中缺血/再灌注诱导的脊髓损伤。

Lipoxin A4 ameliorates ischemia/reperfusion induced spinal cord injury in rabbit model.

作者信息

Liu Zhi-Qiang, Zhang Hong-Bin, Wang Jian, Xia Li-Jian, Zhang Wei

机构信息

Jining Medical College Rizhao, Shandong, China.

Health Center, Shandong Provincial Qianfoshan Hospital Affiliated to Shandong University Jinan, Shandong, China.

出版信息

Int J Clin Exp Med. 2015 Aug 15;8(8):12826-33. eCollection 2015.

Abstract

Ischemia/reperfusion (I/R) induced spinal cord injury is an important pathologic mechanism leading to the paraplegia observed after surgery to repairaortic aneurysms. This study aims to investigate the neuroprotective effects of Lipoxin A4 and its potential mechanism in a rabbit model with I/R spinal cord injury. Forty-five rabbits were randomly divided into three groups: sham group, I/R group and Lipoxin A4 group. Rabbits were subject to 30 min aortic occlusion to induce transient spinal cord ischemia. All animals were sacrificed after neurological evaluation with modified Tarlov criteria at the 48th hour after reperfusion, and the spinal cord segments (L4-6) were harvested for histopathological examination, as well as local malondialdehyde (MDA) and total superoxide dismutase (SOD) activity analysis. All animals in the I/R group became paraplegic. While after 48-hour treatment, compared with I/R group, Lipoxin A4 significantly improved neurological function, reduced cell apoptosis and MDA levels as well as increased SOD activity (P < 0.05). These results suggest that Lipoxin A4 can ameliorate I/R induced spinal cord injury in Rabbit through its antiapoptosis and antioxidant activity.

摘要

缺血/再灌注(I/R)诱导的脊髓损伤是导致主动脉瘤修复手术后截瘫的重要病理机制。本研究旨在探讨脂氧素A4在兔I/R脊髓损伤模型中的神经保护作用及其潜在机制。45只兔子随机分为三组:假手术组、I/R组和脂氧素A4组。对兔子进行30分钟的主动脉阻断以诱导短暂性脊髓缺血。在再灌注后第48小时,根据改良的Tarlov标准进行神经功能评估后处死所有动物,取脊髓节段(L4-6)进行组织病理学检查,以及局部丙二醛(MDA)和总超氧化物歧化酶(SOD)活性分析。I/R组所有动物均出现截瘫。而经过48小时治疗后,与I/R组相比,脂氧素A4显著改善神经功能,降低细胞凋亡和MDA水平,并提高SOD活性(P<0.05)。这些结果表明,脂氧素A4可通过其抗凋亡和抗氧化活性改善兔I/R诱导的脊髓损伤。

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