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Effects of magnetic stimulation on apoptosis of nerve cells and the production of iNOS after spinal cord injury / 中华物理医学与康复杂志
Chinese Journal of Physical Medicine and Rehabilitation ; (12): 10-13, 2011.
Artículo en Chino | WPRIM | ID: wpr-382675
ABSTRACT
Objective To investigate effects of magnetic stimulation on apoptosis of nerve cells and the production of inducible nitric oxidate synthase (iNOS) after spinal cord injury (SCI). Methods Thirty-two SpragueDawley male rats were randomly divided into a magnetic stimulation group (n = 16) and a control group (n = 16).SCI models were established by spinal cord transection in both groups. Rats were sacrificed at the 6th, 12th, 24th and 72nd hour post-injury, but the rats in the stimulation group received magnetic stimulation before being sacrificed.Apoptosis index (AI) and iNOS-positive cells rate were recorded at each time point. Results Apoptotic cells could be observed by the 6th hour post-injury, and were elevated from the 24th to the 72th hour. iNOS-positive cells were few at the first two time points, but had increased significantly at the 24th and 72nd hour post-injury. Compared with the control group, the apoptosis index of the stimulation group decreased a little at the 6th and 12th hour, but not significantly. The difference was quite significant at the 24th and 72nd hour, however, and the AI in the stimulation group decreased much more than that in the control group. There was little difference in the rate of iNOS-positive cells between the control and stimulation groups at any time point. Conclusions Magnetic stimulation could inhibit neural apoptosis and protect neurons from secondary SCI, but it has little effect on iNOS production.

Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Idioma: Chino Revista: Chinese Journal of Physical Medicine and Rehabilitation Año: 2011 Tipo del documento: Artículo

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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Idioma: Chino Revista: Chinese Journal of Physical Medicine and Rehabilitation Año: 2011 Tipo del documento: Artículo