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

被引:24
作者
Garcimartin, Alba [1 ,2 ]
Merino, Jose J. [3 ]
Pilar Gonzalez, Maria [3 ]
Isabel Sanchez-Reus, Maria [3 ]
Sanchez-Muniz, Francisco J. [2 ]
Bastida, Sara [2 ]
Benedi, Juana [1 ]
机构
[1] Univ Complutense Madrid, Fac Farm, Dept Farmacol, E-28040 Madrid, Spain
[2] Univ Complutense Madrid, Fac Farm, Dept Nutr & Bromatol Nutr 1, E-28040 Madrid, Spain
[3] Univ Complutense Madrid, Fac Farm, Dept Bioquim Biol Mol 2, E-28040 Madrid, Spain
来源
BMC COMPLEMENTARY AND ALTERNATIVE MEDICINE | 2014年 / 14卷
关键词
Silicon; Cellular death; LDH; ROS; Caspase-3; -8; -9; Neuroprotection; OXIDATIVE STRESS; ALUMINUM HYPOTHESIS; ALZHEIMERS-DISEASE; DRINKING-WATER; DEATH; ACTIVATION; APOPTOSIS; PATHWAY; RATS;
D O I
10.1186/1472-6882-14-384
中图分类号
R [医药、卫生];
学科分类号
10 ;
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 mu M, 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.
引用
收藏
页数:9
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