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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

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 pathogene...

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Published in:PloS one 2019-03, Vol.14 (3), p.e0214100-e0214100
Main Authors: Hsieh, Chih-Hsiung, Lu, Chueh-Hsuan, Kuo, Yu-Yi, Lin, Guan-Bo, Chao, Chih-Yu
Format: Article
Language:English
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Summary: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.
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0214100