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Neuroprotective Effect of Low Frequency-Pulsed Electromagnetic Fields in Ischemic Stroke

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Urnukhsaikhan E, Mishig-Ochir T, Kim S-C, Park J-K, Seo Y-K · 2017

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C57B6 mice exposed to LF-PEMF at 60 Hz and 10 mT after photothrombotic occlusion showed a neuroprotective effect.

Plain English Summary

Summary written for general audiences

Researchers exposed C57B6 mice to LF-PEMF at 60 Hz and 10 mT after inducing ischemic stroke via photothrombotic occlusion. They measured the BDNF/TrkB/Akt signaling pathway, pro-apoptotic and pro-survival protein and gene expressions, inflammatory mediators, and performed behavioral tests. LF-PEMF treatment promoted activation of the BDNF/TrkB/Akt signaling pathway. Pro-survival proteins increased significantly, while pro-apoptotic proteins and inflammatory mediators decreased. The results demonstrated a neuroprotective effect of LF-PEMF exposure after ischemic stroke in mice during recovery.

Why This Matters

The researchers noted that low frequency-pulsed electromagnetic fields affect many biological processes but their fundamental mechanisms remain unclear. The study aimed to investigate the effect of LF-PEMFs on neuroprotection after ischemic stroke.

Cite This Study
Urnukhsaikhan E, Mishig-Ochir T, Kim S-C, Park J-K, Seo Y-K (2017). Neuroprotective Effect of Low Frequency-Pulsed Electromagnetic Fields in Ischemic Stroke.
Show BibTeX
@article{urnukhsaikhan_e_mishig_ochir_t_kim_s_c_park_j_k_seo_y_k_ce4575,
  author = {Urnukhsaikhan E and Mishig-Ochir T and Kim S-C and Park J-K and Seo Y-K},
  title = {Neuroprotective Effect of Low Frequency-Pulsed Electromagnetic Fields in Ischemic Stroke},
  year = {2017},
  
  
}

Quick Questions About This Study

C57B6 mice were exposed to LF-PEMF at 60 Hz and 10 mT after photothrombotic occlusion.
LF-PEMF treatment promoted activation of the BDNF/TrkB/Akt signaling pathway.
Pro-survival proteins were significantly increased, while pro-apoptotic proteins and inflammatory mediators were decreased.
The results demonstrated that LF-PEMF exposure has a neuroprotective effect after ischemic stroke in mice during the recovery process.