Acute neuroprotective effects of extremely low-frequency electromagnetic fields after traumatic brain injury in rats.

Author: Yang Y, Li L, Wang YG, Fei Z, Zhong J, Wei LZ, Long QF, Liu WP.
Affiliation:
Department of Neurosurgery, Xijing Hospital, The Fourth Military Medical University, 17 West Changle Road, Xi'an 710032, China.
Conference/Journal: Neurosci Lett.
Date published: 2012 Mar 19
Other: Word Count: 242



Traumatic brain injury commonly has a result of a short window of opportunity between the period of initial brain injury and secondary brain injury, which provides protective strategies and can reduce damages of brain due to secondary brain injury. Previous studies have reported neuroprotective effects of extremely low-frequency electromagnetic fields. However, the effects of extremely low-frequency electromagnetic fields on neural damage after traumatic brain injury have not been reported yet. The present study aims to investigate effects of extremely low-frequency electromagnetic fields on neuroprotection after traumatic brain injury. Male Sprague-Dawley rats were used for the model of lateral fluid percussion injury, which were placed in non-electromagnetic fields and 15Hz (Hertz) electromagnetic fields with intensities of 1G (Gauss), 3G and 5G. At various time points (ranging from 0.5 to 30h) after lateral fluid percussion injury, rats were treated with kainic acid (administered by intraperitoneal injection) to induce apoptosis in hippocampal cells. The results were as follows: (1) the expression of hypoxia-inducible factor-1α was dramatically decreased during the neuroprotective time window. (2) The kainic acid-induced apoptosis in the hippocampus was significantly decreased in rats exposed to electromagnetic fields. (3) Electromagnetic fields exposure shortened the escape time in water maze test. (4) Electromagnetic fields exposure accelerated the recovery of the blood-brain barrier after brain injury. These findings revealed that extremely low-frequency electromagnetic fields significantly prolong the window of opportunity for brain protection and enhance the intensity of neuroprotection after traumatic brain injury.
Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.
PMID: 22484017

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