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Repetitive magnetic stimulation affects the microenvironment of nerve regeneration and evoked potentials after spinal cord injury

Repetitive magnetic stimulation affects the microenvironment of nerve regeneration and evoked potentials after spinal cord injury

作     者:Jin-lan Jiang Xu-dong Guo Shu-quan Zhang Xin-gang Wang Shi-feng Wu 

作者机构:Scientific Research Center China-Japan Union Hospital Jilin University Department of Orthopedics China-Japan Union Hospital Jilin University Department of Cardiovascular Medicine China-Japan Union Hospital Jilin University Department of Orthopedics Tianjin Nankai Hospital Department of Burns and Plastic Surgery China-Japan Union Hospital Jilin University 

出 版 物:《Neural Regeneration Research》 (中国神经再生研究(英文版))

年 卷 期:2016年第11卷第5期

页      面:816-822页

核心收录:

学科分类:0710[理学-生物学] 1002[医学-临床医学] 1001[医学-基础医学(可授医学、理学学位)] 10[医学] 

主  题:nerve regeneration spinal cord injury repetitive magnetic stimulation motor function rats rehabilitation plasticity regenerative microenvironment neural regeneration 

摘      要:Repetitive magnetic stimulation has been shown to alter local blood flow of the brain, excite the corticospinal tract and muscle, and induce motor function recovery. We established a rat model of acute spinal cord injury using the modified Allen's method. After 4 hours of injury, rat models received repetitive magnetic stimulation, with a stimulus intensity of 35% maximum output intensity, 5-Hz frequency, 5 seconds for each sequence, and an interval of 2 minutes. This was repeated for a total of 10 sequences, once a day, 5 days in a week, for 2 consecutive weeks. After repetitive magnetic stimulation, the number of apoptotic cells decreased, matrix metalloproteinase 9/2 gene and protein expression decreased, nestin expression increased, somatosensory and motor-evoked potentials recovered, and motor function recovered in the injured spinal cord. These findings confirm that repetitive magnetic stimulation of the spinal cord improved the microenvironment of neural regeneration, reduced neuronal apoptosis, and induced neuroprotective and repair effects on the injured spinal cord.

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