The protective effect of non-invasive low intensity pulsed electric field and fucoidan in preventing oxidative stress-induced motor neuron death via ROCK/Akt pathway

PLoS One. 2019 Mar 19;14(3):e0214100. doi: 10.1371/journal.pone.0214100. eCollection 2019.

Abstract

With the expansion of the aged population, it is predicted that neurodegenerative diseases (NDDs) will become a major threat to public health worldwide. However, existing therapies can control the symptoms of the diseases at best, rather than offering a fundamental cure. As for the complex pathogenesis, clinical and preclinical researches have indicated that oxidative stress, a central role in neuronal degeneration, is a possible therapeutic target in the development of novel remedies. In this study, the motor neuron-like cell line NSC-34 was employed as an experimental model in probing the effects induced by the combination of non-invasive low intensity pulsed electric field (LIPEF) and fucoidan on the H2O2-induced neuron damage. It was found that single treatment of the LIPEF could protect the NSC-34 cells from oxidative stress, and the protective effect was enhanced by combining the LIPEF and fucoidan. Notably, it was observed that single treatment of the LIPEF obviously suppressed the H2O2-enhanced expression of ROCK protein and increased the phosphorylation of Akt in the H2O2-treated NSC-34 cells. Moreover, the LIPEF can be easily modified to concentrate on a specific area. Accordingly, this technique can be used as an advanced remedy for ROCK inhibition without the drawback of drug metabolism. Therefore, we suggest the LIPEF would be a promising strategy as a treatment for motor neurodegeneration and warrant further probe into its potential in treating other neuronal degenerations.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Death / drug effects
  • Cell Line
  • Electric Stimulation Therapy*
  • Humans
  • Mice
  • Motor Neurons / metabolism*
  • Motor Neurons / pathology
  • Neurodegenerative Diseases / metabolism
  • Neurodegenerative Diseases / pathology
  • Neurodegenerative Diseases / therapy
  • Oxidative Stress / drug effects*
  • Polysaccharides / pharmacology*
  • Proto-Oncogene Proteins c-akt / metabolism*
  • Signal Transduction / drug effects*
  • rho-Associated Kinases / metabolism*

Substances

  • Polysaccharides
  • fucoidan
  • Proto-Oncogene Proteins c-akt
  • rho-Associated Kinases

Grants and funding

This work was supported by grants from Ministry of Science and Technology (MOST 105-2112-M-002-006-MY3 to CYC) and Ministry of Education (MOE 107L880406 to CYC) of the Republic of China. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.