金刚烷胺在兔脊髓缺血再灌注模型中的神经保护作用

Caner Unluer, Pinar Kuru Bektasoglu, Berrin Imge Erguder, Ata Turker Arikok, Ilcim Ermutlu, Bora Gurer, Hayri Kertmen
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引用次数: 0

摘要

目的:本研究采用实验性兔脊髓缺血再灌注损伤(SCIRI)模型,探讨具有神经保护和抗炎活性的药物金刚烷胺对氧化应激、组织坏死、细胞凋亡和神经功能恢复的影响:将兔子随机分为五组:对照组、缺血组、载体组、甲基强的松龙组(MP)和金刚烷胺组(AMT)。第24小时进行神经系统检查,收集脊髓组织并进行生化和组织病理学检查:缺血组和药物组与对照组相比,血清和组织中的 Caspase-3、丙二醛(MDA)和髓过氧化物酶(MPO)水平显著升高(P 0.001);血清和组织中的过氧化氢酶(CAT)水平显著降低(P 0.001);血清中的黄嘌呤氧化酶(XO)水平显著升高(P 0.001)。缺血组与 MP 组和 AMT 组比较,发现血清和组织中 caspase-3 水平低(p 0.001),血清和组织中 CAT 水平高(p 0.001),血清 XO 水平显著低(p 0.001),血清和组织中 MDA 水平低(p 0.05),组织中 MPO 水平低(p 0.001)。与缺血组相比,AMT 组和 MP 组的组织病理学评分均有所下降,正常神经元数量增加(P 0.001)。与缺血组相比,AMT 组和 MP 组都显示出更好的改良 Tarlov 评分(P 0.001):在这项研究中,我们首次在文献中利用生化、显微镜和超微结构技术证明了 AMT 对 SCIRI 的抗氧化、抗炎、抗凋亡和神经保护作用。AMT 可能是预防和治疗 SCIRI 的候选药物。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Amantadine's Neuroprotective Effects in Rabbit Spinal Cord Ischemia/Reperfusion Model.

Aim: To examine the effects of amantadine, a drug with neuroprotective and anti-inflammatory activities on oxidative stress, tissue necrosis, apoptosis, and neurological recovery in an experimental rabbit spinal cord ischemia-reperfusion injury (SCIRI) model.

Material and methods: A total of 32 rabbits were randomized into five groups: control, ischemia, vehicle, methylprednisolone (MP), and amantadine (AMT) (n=8/each). At 24th-hour neurological examination was performed, spinal cord tissues were collected, and biochemical and histopathological examinations were performed.

Results: When ischemia and vehicle groups were compared with control group, significant increase was seen in serum and tissue caspase-3, malondialdehyde (MDA), and myeloperoxidase (MPO) levels (p < 0.001); significant decrease was seen in serum and tissue catalase (CAT) levels (p < 0.001); and significant increase was seen in serum xanthine oxidase (XO) levels (p < 0.001). When the ischemia group and the MP and AMT groups were compared, low serum and tissue caspase-3 levels (p < 0.001), high serum and tissue CAT levels (p < 0.001), significantly low serum XO levels (p < 0.001), low serum and tissue MDA levels (p < 0.05) and tissue MPO levels (p < 0.001) were found. Both AMT and MP groups showed decreased histopathological score and higher number of normal neurons (p < 0.001) compared to ischemia group. Both AMT and MP showed better modified Tarlov scores compared to the ischemia group (p < 0.001).

Conclusion: Our study found that AMT had antioxidant, anti-inflammatory, anti-apoptotic, and neuroprotective effects on SCIRI. We used biochemical, microscopic, and ultrastructural approaches to demonstrate these effects. AMT might be a candidate medication for SCIRI prophylaxis and treatment.

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