Extremely low frequency pulsed electromagnetic fields cause antioxidative defense mechanisms in human osteoblasts via induction of •O2? and H2O2

Disclaimer: this research study’s copyright belongs to the authors and PubMed and not HealthMatReview.com, further details below.

Our Summary

We previously demonstrated that extremely low-frequency pulsed electromagnetic field (ELF-PEMF) stimulated human osteoblast (hOBs) function having reactive oxygen species (ROS) as process regulators. This study now investigates the effect of ELF-PEMF on the modulation of hOBs function via ROS. Results showed ELF-PEMF affected differentiation of hOBs that leads to the induction of antioxidative defense mechanisms which suggests possible beneficial effects on one formation under oxidative stress conditions.

Pubmed Study Link

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5673962/

PDF Study Link

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5673962/pdf/41598_2017_Article_14983.pdf

Study Categories

bone healing, brittle bone

Authors

[‘Sabrina Ehnert’, ‘Anne-Kristin Fentz’, ‘Anna Schreiner’, ‘Johannes Birk’, ‘Benjamin Wilbrand’, ‘Patrick Ziegler’, ‘Marie K. Reumann’, ‘Hongbo Wang’, ‘Karsten Falldorf’, ‘Andreas K. Nussler’]

PMID

29109418

PMCID

PMC5673962

Published Date

more study details

Frequency (Hz)

16

Frequency Range

Low

Intensity (G)

0.06, 2.82

Intensity Range

Low

Waveform

unknown

PEMF/EMF/RF/LT

ELF-PEMF

Study Subject Types

human

Keywords Listed

Added Descriptive Keywords

bone, bone matrix, mineralization, bone marrow, bone regeneration, brittle bone, human

Disclaimer

All intellectual property and copyright of this research study sourced from PubMed, is the property of the authors and associates and is not the property of HealthMatReview.com. This research study has been included in our custom PEMF research database for the educational purposes of our readers. The on page summary, added descriptive keywords and other study details are copyright of HealthMatReview.com and were added to improve the search function of this custom research database.

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