Polyethylene glycol immediately repairs neuronal membranes and inhibits free radical production after acute spinal cord injury
Polyethylene glycol immediately repairs neuronal membranes and inhibits free radical production after acute spinal cord injury
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DOI：
10.1046/j.1471-4159.2002.01160.x
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发表时间：
2002-10-01
影响因子：
4.7
通讯作者：
Shi, R
中科院分区：
文献类型：
--
作者：
Luo, J;Borgens, R;Shi, R
创伤性脊髓损伤后，神经细胞及其突起的膜破坏和ROS的产生是导致即刻功能丧失、进行性变性和死亡的重要因素。利用豚鼠体外脊髓损伤模型，我们证明了亲水性聚合物聚乙二醇能显著加速和增强膜的再密封过程，从而在受控压缩后恢复膜的完整性。PEG处理显著抑制了伤害诱导的ROS升高和脂质过氧化(LPO)水平。我们进一步证明，聚乙二醇不是一种有效的自由基清除剂，也没有能力抑制黄嘌呤氧化酶，黄嘌呤氧化酶是产生超氧化物的关键酶。这些观察结果表明，是聚乙二醇介导膜修复导致了ROS和LPO的抑制。此外，我们的数据还暗示了在脊髓损伤中膜破坏在ROS产生中的重要原因，提示膜修复是减少ROS发生的有效靶点。
Membrane disruption and the production of reactive oxygen species (ROS) are important factors causing immediate functional loss, progressive degeneration, and death in neurons and their processes after traumatic spinal cord injury. Using an in vitro guinea pig spinal cord injury model, we have shown that polyethylene glycol (PEG), a hydrophilic polymer, can significantly accelerate and enhance the membrane resealing process to restore membrane integrity following controlled compression. As a result of PEG treatment, injury-induced ROS elevation and lipid peroxidation (LPO) levels were significantly suppressed. We further show that PEG is not an effective free radical scavenger nor does it have the ability to suppress xanthine oxidase, a key enzyme in generating superoxide. These observations suggest that it is the PEG-mediated membrane repair that leads to ROS and LPO inhibition. Furthermore, our data also imply an important causal effect of membrane disruption in generating ROS in spinal cord injury, suggesting membrane repair to be an effective target in reducing ROS genesis.