Dogan Guvenc, Karaca Onur
Hitit University, School of Medicine, Department of Anesthesiology and Reanimation, Corum, Turkey.
Turk Neurosurg. 2020;30(1):60-68. doi: 10.5137/1019-5149.JTN.26801-19.3.
To investigate the neuroprotective effect of a N-methyl-D-aspartate (NMDA) receptor antagonist (amantadine) in an experimental spinal cord injury (SCI) model.
Thirty male Spragueâ€"Dawley rats were divided into three groups: control (I), SCI (II), and SCI + amantadine (III). SCI was created using clip compression technique. At the end of day 7, blood samples were obtained from the rats and analyzed using various biochemical markers. Histological examination was also performed. MDA, GSH, and MPO assays were done. VEGF, TNF-α, and Baxexpressions were also analyzed.
The group III had several inflammatory cells in the gray and white matter, with mildly degenerated multipolar and bipolar cells. Some bipolar and multipolar neurons showed TNF-α expression; however, TNF-α was found to be weak in small groups of inflammatory cells around the blood vessels in the substantia grisea and alba. Positive Bax expression was observed in the substantia grisea layer, particularly in the membrane of some bipolar neurons and glial cells; however, negative Bax expression was observed in neuron and glial cells and showed positive VEGF expression in the vascular endothelium in the group III.
NMDA receptor antagonists, especially amantadine, may ameliorate SCI by inducing angiogenesis, affecting inflammation and apoptosis. It inhibits oxidative stress and the signaling pathways following SCI in rats.
研究N-甲基-D-天冬氨酸（NMDA）受体拮抗剂（金刚烷胺）在实验性脊髓损伤（SCI）模型中的神经保护作用。
将30只雄性Sprague-Dawley大鼠分为三组：对照组（I）、脊髓损伤组（II）和脊髓损伤+金刚烷胺组（III）。采用夹压技术造成脊髓损伤。在第7天结束时，采集大鼠血样并使用各种生化标志物进行分析。还进行了组织学检查。进行了丙二醛（MDA）、谷胱甘肽（GSH）和髓过氧化物酶（MPO）检测。还分析了血管内皮生长因子（VEGF）、肿瘤坏死因子-α（TNF-α）和Bax的表达。
III组在灰质和白质中有多个炎症细胞，多极和双极细胞轻度退化。一些双极和多极神经元显示TNF-α表达；然而，在灰质和白质中血管周围的小群炎症细胞中发现TNF-α较弱。在灰质层观察到Bax阳性表达，特别是在一些双极神经元和神经胶质细胞膜中；然而，在III组的神经元和神经胶质细胞中观察到Bax阴性表达，并且在血管内皮中显示VEGF阳性表达。
NMDA受体拮抗剂，尤其是金刚烷胺，可能通过诱导血管生成、影响炎症和细胞凋亡来改善脊髓损伤。它抑制大鼠脊髓损伤后的氧化应激和信号通路。
