Molecular Mechanism And Brain Injury Of PEMF-Induced BBB Permeability Change In Rats

To investigate the molecular mechanism and brain Injury with PulseElectromagnetic Field induced BBB permeability change in Rats, BBB permeabilitywas measured by Evans-Blue extravasation. The expressions of Occludin, ZO-1,MMP-2and MMP-9were detected by real-time quantitative reverse transcriptase-PCRand western blotting. MMP-2and MMP-9activity were detected by EnzChek gelatinaseassay. To investigate whether PEMF exposure for opening the BBB causes any damageof CNS in rats, the expressions of CaMKIIβ and NMDAR-1were detected by real-timequantitative reverse transcriptase-PCR and western blotting. S100B protein level inserum was determined by Enzyme-linked immunosorbent assay and expression level inbrain tissues was detected by western blotting. PEMF induces neuronal death in the ratcortex was measured by terminal dUTP transferase-mediated nick end-labeling. Toinvestigate the alteration of fluoresence emission spectra and infrared absorption spectraof serum of rats after exposure on PEMF, a spectral collected by fluorescence spectraand recorded by Nicolet760FTIR at different time points after PEMF exposure.The results are listed as follow:1. Compared with sham group, PEMF exposure led to increase permeability of theBBB to EB. Changes of BBB permeability were related to the alteration expression oftight junction proteins and matrix metalloproteinase after exposure to PEMF. BBBpermeability was selective increases after exposure on PEMF, which was related to theexpression levels of Occludin and ZO-1were selectively decreased, MMP-2andMMP-9were selectively increased.2. Compared with sham group, PEMF exposure led to increase GFAP, S100B,Bcl-2expression. The results showed electromagnetic fields affect brain function,structural and metabolic, but the expression of Bcl-2increased to reduce the death of thedamaged nerve cells to alleviate the brain damage. Compared with sham group, theexpression levels of NMDAR and CaMKIIβ were selectively decreased after exposureon PEMF, and recovery to normal levels at6h, which was related to learning andmemory. The cell apoptosis and NMDA signaling were regulated by the JNK pathway of MAPK signaling path.3. A spectral collected by infrared spectra and fluorescence spectra in serum of ratsafter exposure on PEMF. The results showed some significant differences between theexposed groups and the sham exposed group. The helix in protein secondary structurewere reduced, the structural stability was decreased after exposure on PEMF, whichaffect the biological activity of the protein molecule. These differences are mainlycaused by changes in composition and structure of micro-molecules and changes ofvibrational modes of the proteins. The absorption peaks and fluorescence intensity inserum of rats after exposure on PEMF were significantly increased. These findingindicate that the biological damage effects induced by200pulse electromagnetic fieldwere lower than400pulse with3.5ns rising time,7ns pulse half-width, and amplitudeup to200kV at1Hz repetitive rate, which can be used as the optimal pulse conditions.