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Published in: BMC Complementary Medicine and Therapies 1/2014

Open Access 01-12-2014 | Research article

Organic silicon protects human neuroblastoma SH-SY5Y cells against hydrogen peroxide effects

Authors: Alba Garcimartín, José J Merino, Maria Pilar González, Maria Isabel Sánchez-Reus, Francisco J Sánchez-Muniz, Sara Bastida, Juana Benedí

Published in: BMC Complementary Medicine and Therapies | Issue 1/2014

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Abstract

Background

Hydrogen peroxide (H2O2) is a toxic agent that induces oxidative stress and cell death. Silicon (Si) is a biological element involved in limiting aluminium (Al) absorption with possible preventive effects in Alzheimer’s disease. However, Si has not yet been associated with other neuroprotective mechanisms.

Methods

The present experiments evaluated in the SH-SY5Y human neuroblastoma cell line the possible role of different Si G5 (50-1000 ng/mL) concentrations in preventing cellular death induced by H2O2 (400 μM, 24 hours).

Results

Our findings showed that H2O2 promoted cell death in the human SH-SY5Y cell cultures and this could be prevented by Si treatment. The loss in cell viability mediated by H2O2 was due to an apoptotic and necrotic process. Apoptotic death was incurred by regulating caspase-8 activity in the extrinsic pathway. The apoptotic and necrotic cell death induced by H2O2 was almost totally reversed by Si (50-500 ng/mL), indicating that it down-regulates both processes in H2O2 treated cells.

Conclusions

According to our data, Si is able to increase SH-SY5Y cell survival throughout partially blocking cellular damage related to oxidative stress through a mechanism that would affect H2O2/ROS elimination.
Appendix
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Metadata
Title
Organic silicon protects human neuroblastoma SH-SY5Y cells against hydrogen peroxide effects
Authors
Alba Garcimartín
José J Merino
Maria Pilar González
Maria Isabel Sánchez-Reus
Francisco J Sánchez-Muniz
Sara Bastida
Juana Benedí
Publication date
01-12-2014
Publisher
BioMed Central
Published in
BMC Complementary Medicine and Therapies / Issue 1/2014
Electronic ISSN: 2662-7671
DOI
https://doi.org/10.1186/1472-6882-14-384

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