神经营养素-3对大鼠急性脊髓损伤后血中SOD和MDA的影响

Effect of Neurotrophin-3 on SOD and MDA after acutal spinal cord injury in blood of rats.

目的观察NT-3对大鼠急性脊髓损伤后血中SOD和MDA水平的影响,并从自由基和脂质过氧化角度来探讨其对急性脊髓损伤的保护作用机制。方法105只SD大鼠随机分成3组:对照组(生理盐水组),实验组(NT-3组)和假手术组。用改良Allen’s WD法以6g×5cm致伤SD大鼠制作大鼠全瘫模型,经蛛网膜下隙导管于术后即刻,4,8,12,24h,3,7d注入NT-3 20μl(含NT-3 200ng),对照组在相同时间点给予等量生理盐水,假手术组只打开椎板后蛛网膜下隙置管,不致伤,不给药。术后4,8,12,24h,3,7,14d取血离心,利用分光光度计测定SOD和MDA吸光度来检测其变化。结果脊髓损伤后SOD水平降低,损伤后3d达最低水平,以后略有回升,脊髓损伤后MDA水平升高,伤后7d达高峰,以后逐渐下降;实验组SOD水平显著高于对照组(P<0.01),MDA水平明显低于对照组(P<0.01),大鼠运动功能恢复也明显优于对照组。结论NT-3能提高SOD水平和降低MDA水平,减少自由基和脂质过氧化的损伤,从而保护脊髓组织,这可能是NT-3对脊髓损伤具有保护作用的机制之一。

Objective To investigate the effect of NT-3 on the expressional level of SOD and MDA in the injured spinal cord of rats. Methods Using the method of Allen＇s WD to make the animal model of acute spinal cord injured of rats, 105 SD rats were randomly divided into three groups, control group, experimental group and sham group. A thin plastic tube was situated in subarachnoid space below the injury level for perfusion. Rats in experimental group received NT-3 20μl（ including NT-3 200ng）from the tube at oh 4h, 8h, 12h, 24h and 3d, 7d, after injury. The saline-treated animals received the volume of normal saline at the same time as control. The animals in sham group only received opening vertebral plate and putting tube in subarachnoid space, the rats were sacrificed at 4h, 8h, 12h, 24 and 3d,7d, 14d postinjury（ n = 5）and the levels of SOD and MDA in blood were observed with colorimetric methods. Results The level of SOD was reduced obviously and the level of MDA was raised obviously in its serum, the activity of SOD reached the lowest at the 3d and the concentration of MDA reached peak at the 7d. In the experimental NT-3 can help the spinal function recover. Conclusion NT- 3 can protect spinal cord from injury in vivo. One of mechanisms is that inhibits abnormal expression of malondialdehyde（MDA） and elevate the activity of Superoxide Dismutase（ SOD）, thus the injury of free radical and lipid peroxidation is attenuated.