摘要
急性脊髓损伤可导致严重的运动、感觉功能障碍,由自由基引起的氧化应激在继发性脊髓损伤的病理生理过程中占有重要地位。通过有效的抗氧化干预抑制损伤后生物大分子的过氧化反应,将成为药物治疗脊髓损伤的一条策略。本文主要介绍氧化应激的产生原因、作用过程和参与急性脊髓损伤的病理生理机制,并综述抗氧化药物实验研究的最新进展,旨在为寻找安全有效的药物提供参考依据。
Acute spinal cord injury can lead to severe motor and sensory dysfunction. Oxidative stress caused by free radical plays an important role in the pathophysiology of secondary injury. Inhibition of biological macromolecules peroxidation damage through antioxidant intervention may be an effective strategy for drug therapy of spinal cord injury. This paper mainly introduces the cause,process and participation of oxidative stress in the pathophysiological mechanism of acute spinal cord injury,and also reviews the recent advances in antioxidant drug research,aiming to facilitate the discovery of safe and effective antioxidant drugs for potential treatment of acute spinal cord injury.
出处
《神经药理学报》
2012年第3期52-64,共13页
Acta Neuropharmacologica
基金
国家自然科学基金资助项目(No.30960448)
江西省自然科学基金项目(No.20114BAB205033)
江西省教育厅科技项目(No.GJJ11596)
关键词
脊髓损伤
氧化应激
抗氧化
spinal cord injury
oxidative stress
antioxidant
