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实验性脊髓损伤中的神经元和轴突变性:体内质子磁共振波谱和组织学。

Neuronal and axonal degeneration in experimental spinal cord injury: in vivo proton magnetic resonance spectroscopy and histology.

机构信息

Department of Diagnostic and Interventional Imaging, The University of Texas Medical School at Houston, Houston, Texas 77030, USA.

出版信息

J Neurotrauma. 2010 Mar;27(3):599-610. doi: 10.1089/neu.2009.1145.

Abstract

Longitudinal in vivo proton magnetic resonance spectroscopy (1H-MRS) and immunohistochemistry were performed to investigate the tissue degeneration in traumatically injured rat spinal cord rostral and caudal to the lesion epicenter. On 1H-MRS significant decreases in N-acetyl aspartate (NAA) and total creatine (Cr) levels in the rostral, epicenter, and caudal segments were observed by 14 days, and levels remained depressed up to 56 days post-injury (PI). In contrast, the total choline (Cho) levels increased significantly in all three segments by 14 days PI, but recovered in the epicenter and caudal, but not the rostral region, at 56 days PI. Immunohistochemistry demonstrated neuronal cell death in the gray matter, and reactive astrocytes and axonal degeneration in the dorsal, lateral, and ventral white-matter columns. These results suggest delayed tissue degeneration in regions both rostrally and caudally from the epicenter in the injured spinal cord tissue. A rostral-caudal asymmetry in tissue recovery was seen both on MRI-observed hyperintense lesion volume and the Cho, but not NAA and Cr, levels at 56 days PI. These studies suggest that dynamic metabolic changes take place in regions away from the epicenter in injured spinal cord.

摘要

进行了纵向体内质子磁共振波谱(1H-MRS)和免疫组织化学研究,以调查创伤性损伤大鼠脊髓损伤中心上下的组织退化。在 1H-MRS 上,通过 14 天观察到损伤中心上下的 N-乙酰天冬氨酸(NAA)和总肌酸(Cr)水平显着降低,并且直到损伤后 56 天(PI)水平仍保持降低。相比之下,在所有三个节段中,总胆碱(Cho)水平在 14 天 PI 时均显着增加,但在 56 天 PI 时仅在损伤中心和尾部恢复,而在头部区域则没有恢复。免疫组织化学显示灰质中的神经元细胞死亡,以及背侧、外侧和腹侧白质柱中的反应性星形胶质细胞和轴突变性。这些结果表明,损伤脊髓组织中损伤中心上下的区域存在延迟的组织退化。在 56 天 PI 时,不仅在 MRI 观察到的高信号病变体积上,而且在 Cho,但不是 NAA 和 Cr 水平上,都观察到组织恢复的头尾部不对称性。这些研究表明,在损伤的脊髓远离损伤中心的区域中发生了动态代谢变化。

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