Ischemic strokes were experimentally induced in male mice. After the stroke, mice were divided into 2 groups (n=18 each): 1) exposure to the magnetic field and 2) sham exposure. Mice from each group were killed after 1, 3 and 14 days of exposure (remark EMF-Portal: respective numbers were not stated).
|magnetic flux density||10 mT||-||calculated||-||-|
Exposed mice had significantly longer rotarod times compared to sham exposed mice, indicating better motoric functions.
Previous studies suggested that BDNF and protein kinase C play a central role in neuroprotection, which was confirmed in this study by a significantly increased expression of BDNF, TrkB and phosphorylated protein kinase B in exposed mice compared to sham exposed mice after 3 and 14 days. This resulted further in a significant decrease of gene expression and protein expression of pro-apoptotic Bad, Bax, caspase 3 and a significant increase of anti-apoptotic Bcl-xL expression in the exposure group compared to the sham exposure group.
Moreover, the protein expression of inflammatory mediators MMP9 and IL-1β was significantly decreased in exposed mice compared to sham exposed mice after 3 and 14 days of exposure.
The authors conclude that exposure of mice to a pulsed 60 Hz magnetic field might have a neuroprotective effect after ischemic stroke via suppression of inflammation and apoptosis. They propose that low frequency pulsed electromagnetic fields may be beneficial as a treatment during recovery after ischemic stroke.