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

BMC Complementary and Alternative Medicine

Juana Benedí²  Sara Bastida³  Francisco J Sánchez-Muniz³  Maria Isabel Sánchez-Reus¹  Maria Pilar González¹  José J Merino¹  Alba Garcimartín³ 

[1]Departamento de Bioquímica y Biología Molecular II, Facultad de Farmacia, Universidad Complutense de Madrid, 28040 Madrid, Spain

[2]Depatamento de Farmacología, Facultad de Farmacia, Universidad Complutense de Madrid, 28040 Madrid, Spain

[3]Departamento de Nutrición y Bromatología I (Nutrición), Facultad de Farmacia, Universidad Complutense de Madrid, 28040 Madrid, Spain

关键词: Neuroprotection;    Caspase-3,-8,-9;    ROS;    LDH;    Cellular death;    Silicon;   

Others  :  1086291
DOI  :  10.1186/1472-6882-14-384

 received in 2014-06-30, accepted in 2014-09-29,  发布年份 2014

【 摘 要 】

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.

【 授权许可】

   
2014 Garcimartín et al.; licensee BioMed Central Ltd.

【 图 表 】

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