Abstract

Objective
 Cerebrovascular accident due to ischemia (IS)
 mediated by atherosclerotic plaque in the brain
 can trigger inflammation in the cerebral cortex,
 hippocampus and cerebellum tissues. Radiofrequency
 electromagnetic field (RF-EMF) and pulsed magnetic
 field (PMF) applications can increase nitric oxide
 formation from the vascular endothelial layer. The
 aim of this preliminary study is to reduce the damage
 caused by IS in different tissues of the brain by
 magnetic field applications.
 Material and Method
 A total of 9 rats, one rat in each group; sham,
 prophylactic RF, PMF, RF+PMF and therapeutic
 RF-EMF, PMF, RF-EMF+PMF, prophylactic and
 therapeutic RF-EMF+PMF and IS-only groups were
 distinguished. In single or combined applications of
 prophylactic/therapeutic RF-EMF and PMF groups,
 rats were taken to the experimental unit for 30
 minutes of magnetic field exposure before and after
 30 minutes of carotid artery occlusion for IS purposes.
 Histopathological hematoxylin-eosin staining in
 brain tissue (cerebral cortex and hippocampus)
 and cerebellum tissues taken after sacrification;
 With immunohistochemical analysis, brain derived
 neurotrophic factor (BDNF), tumor necrosis factoralpha
 (TNF-α), mammalian target of rapamycin
 (mTOR) and inducible nitric oxide synthase (iNOS)
 expressions were examined.
 Results
 Histopathologically significant hyperemia, edema,
 bleeding and neuronal degeneration were detected
 in the IS group. Additionally, immunohistochemically,
 an increase in TNF-α, mTOR, iNOS and a decrease
 in BDNF staining were observed. Prophylactic and/or
 therapeutic RF-EMF and/or PMF applications reversed
 all these parameters. The greatest improvement
 was observed in the Prophylactic+Therapeutic RFEMF+
 PMF group.
 Conclusion
 As a result, the regression of IS-related inflammation in
 both brain tissue parts and cerebellar tissues with RFEMF
 and PMF is important in terms of the formation
 of neurological deficits, the continuity of learning
 and memory mechanisms, and the preservation of
 balance functions.

Full Text
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