BACKGROUND:Lipoic acid, with a closed circle structure composed by sulphur and carbon atoms, exerts strong anti-oxidation, and has been extensively applied in the prevention and treatment of oxidative stress, diabetic cataract, diabetic neuropathy and cardiovascular diseases. OBJECTIVE:To investigate the protective effect of lipoic acid on peripheral nerve function during peripheral nerve ischemia/reperfusion injury. METHODS:Models of peripheral nerve ischemia/reperfusion injury were established in rabbits, and then rabbit models were then allotted to treatment and non-treatment groups. The treatment group was subdivided into experimental (injection of lippoic acid) and control groups according to the use of lipoic acid at 1, 3 and 6 hours after ischemia and before reperfusion. The ultrastructural changes of the sciatic nerve were observed under electron microscope, and the electrophysiological changes of the sciatic nerve were detected using evoked potential instrument. RESULTS AND CONCLUSION:With the ischemic time increasing, the number of vacuoles in the axon increased gradually, accompanied by axonal atrophy, and Waller's degeneration in the aggregated microfilaments. The myelin sheath thickening and dissolving were visible. All above phenomena became severest at 6 hours after ischemia. Compared with the control groups, lipoic acid reduced the number of the vacuoles in the axon and all eviated axonal atrophy, Waller's degeneration and demyelination. As the ischemic time increasing, the latency of sciatic nerve was significantly increased, and peaked at 6 hours of ischemia;while the amplitude was significantly decreased, and reached a minimum at 6 hours of ischemia. Compared with the control groups, in the experimental groups, the latency of sciatic nerve was significantly decreased, but the amplitude was significantly increased. These results suggest that lipoic acid provides neuroprotection against peripheral nerve ischemia/reperfusion injury.%背景:硫辛酸具有由硫、碳原子所构成的封闭环状结构,具有强大的抗氧化能力,现已被广泛用于氧化应激、糖尿病性白内障、糖尿病多发性神经病及心血管损伤等糖尿病并发症等疾病的预防和治疗.目的:探究硫辛酸在周围神经缺血再灌注损伤中对周围神经功能的保护作用.方法:建立家兔周围神经缺血再灌注损伤模型,依据是否进行再灌注分为处理组与未处理组(不进行再灌注处理),处理组依据缺血时间1,3,6 h和再灌注前是否使用硫辛酸,于每个时间点又分别分为实验组与对照组,电镜观察各组实验动物坐骨神经超微结构的变化,并使用诱发电位仪检测坐骨神经电生理指标的变化.结果与结论:①随着缺血时间延长,轴突内空泡逐渐增多,轴突发生萎缩,轴突内微丝结构发生聚集并出现了明显的沃勒变性,而髓鞘则出现了增厚紊乱以及溶解现象.超微结构的破坏在缺血6h时最为严重,沃勒变性及髓鞘溶解现象明显增加.对比实验组与对照组,硫辛酸的应用减少坐骨神经轴突中空泡数量,减轻了轴突的萎缩、沃勒变性以及脱髓鞘现象的产生;②随着缺血时间延长,各组实验动物坐骨神经的潜伏期显著增加,而波幅显著降低.潜伏期在缺血6h达到最大值,而波幅在缺血6h达到了最小值.对比未使用硫辛酸的对照组,实验组坐骨神经潜伏期明显下降而波幅明显增加;③结果说明,硫辛酸能够改善缺血再灌注造成的周围神经功能损伤.
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