Fujimoto T, Nakamura T, Ikeda T, Taoka Y, Takagi K
Department of Orthopedic Surgery, Kumamoto University School of Medicine, Japan.
Spine (Phila Pa 1976). 2000 Jan;25(1):24-9. doi: 10.1097/00007632-200001010-00006.
A study in which levels of lipid peroxidation were measured, the thiobarbituric acid-reactive substances were estimated in an experimental rat model, and the recovery was assessed.
To ascertain the occurrence of thiobarbituric acid-reactive substances in the damaged spinal cord, and to investigate the effectiveness of a hydroxyl radical scavenger EPC-K1, a phosphate diester linkage of vitamins E and C, in attenuating the severity of spinal cord injury.
Lipid peroxidation has been reported to play an important role in spinal cord injury. There is no report on the use of EPC-K1 to attenuate the severity of spinal cord injury in either animal or human studies.
Spinal cord injury was induced by placing a 25-g weight on T12, and the animals were divided into six groups. Group 1 (sham) received only laminectomy. Group 2 (control) received spinal cord injury. Group 3 received EPC-K1 5 minutes before injury. Group 4 received it 5 minutes after injury. Group 5 received it 3 hours after injury. Group 6 received it five times, respectively: at 5 minutes, then 1, 2, 3, and 4 hours after injury. The levels of thiobarbituric acid-reactive substances were measured in the spinal cord, and the recovery was assessed.
The thiobarbituric acid-reactive substances content increased after injury, with two peaks, at 1 and 4 hours. Concentration at the 4-hour peak was lower in nitrogen mustard-induced leukocytopenia rats than in the control rats. The EPC-K1 injection reduced thiobarbituric acid-reactive substances content at 1 and 4 hours after injury in Group 3 (respectively, 34.3% and 42.7% vs. control) and only that at 4 hours in Group 6 (24.9% vs. control). Motor function recovery and histologic findings were better in these two groups than in Group 2.
Repeated injection of EPC-K1 attenuated the severity of spinal cord injury.
一项测量脂质过氧化水平、在实验大鼠模型中估计硫代巴比妥酸反应性物质并评估恢复情况的研究。
确定受损脊髓中硫代巴比妥酸反应性物质的出现情况,并研究一种羟基自由基清除剂EPC-K1(维生素E和C的磷酸二酯键合物)在减轻脊髓损伤严重程度方面的有效性。
据报道脂质过氧化在脊髓损伤中起重要作用。在动物或人体研究中,尚无关于使用EPC-K1减轻脊髓损伤严重程度的报道。
通过在T12放置一个25克的重物诱导脊髓损伤,将动物分为六组。第1组(假手术组)仅接受椎板切除术。第2组(对照组)接受脊髓损伤。第3组在损伤前5分钟接受EPC-K1。第4组在损伤后5分钟接受。第5组在损伤后3小时接受。第6组分别在损伤后5分钟、1小时、2小时、3小时和4小时接受五次注射。测量脊髓中硫代巴比妥酸反应性物质的水平,并评估恢复情况。
损伤后硫代巴比妥酸反应性物质含量增加,有两个峰值,分别在1小时和4小时。氮芥诱导的白细胞减少症大鼠在4小时峰值时的浓度低于对照组大鼠。EPC-K1注射降低了第3组损伤后1小时和4小时的硫代巴比妥酸反应性物质含量(分别比对照组降低34.3%和42.7%),以及第6组仅在4小时时的含量(比对照组降低24.9%)。这两组的运动功能恢复和组织学结果均优于第2组。
重复注射EPC-K1可减轻脊髓损伤的严重程度。