High Concentration of Sodium Metasilicate Impairs Autophagic Flux and Induces Apoptosis in Human Umbilical Vein Endothelial Cells

  • Zheng Li
  • Shuhao Liu
  • Yuanwu Cao
  • Tengfei Fu
  • Libo Jiang
  • Jian ZhangEmail author


Silicon-doped materials have been widely used in bone regeneration research; however, a consensus on the safety range of silicon ions has not been reached and its toxicity mechanism remains to be further elucidated. This study aims to explore whether high level of sodium metasilicate can induce toxicity effect in human umbilical vein endothelial cells (HUVEC) and the role of autophagy and apoptosis in its toxic mechanism. HUVEC was treated with different level of high silicon and then investigated with respect to morphologic change, cell viability, immunofluorescence, the level of autophagy, and apoptosis-related protein. Moreover, bafilomycin A1 (Baf A1) was applied to detect whether autophagic flux is disrupted, and 3-methyladenine (3-MA, an autophagy inhibitor) was used to determine the relationship between autophagy and apoptosis. Results demonstrated that high-level silicon induced cell viability to decrease; LC3-II, p62, and apoptosis-related proteins were up-regulated after exposure to high-dose silicon (sodium metasilicate concentration more than 1 mM). There is no significant difference in LC3-II and p62 between Baf A1 and sodium metasilicate-exposed group. Besides, 3-MA further increased the apoptotic rate by inhibiting autophagy after high silicon exposure. Collectively, high concentration of silicon can impair autophagy and induce apoptosis in human umbilical vein endothelial cells, and autophagy may play a protective role in HUVEC apoptosis. Furthermore, silicon concentration used in HUVEC should not be more than 1 mM.


Sodium metasilicate Human umbilical vein endothelial cells Autophagic flux Apoptosis Bafilomycin A1 3-MA 



Human umbilical vein endothelial cell


Cell Counting Kit-8


Bcl-2 associated X protein


Poly ADP-ribose polymerase


Light chain 3



Baf A1

Bafilomycin A1


Inductively coupled plasma atomic emission spectrometry





We appreciate the instruction work by professor Changsheng Liu and his fellow from East China University of Science and Technology.

Funding Information

This work was supported by the Key Project of Natural Science Foundation of China (Grant No. 31330028)

Compliance with Ethical Standards

Conflict of Interest

The authors declare that they have no conflict of interest.


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Copyright information

© Springer Science+Business Media, LLC, part of Springer Nature 2019

Authors and Affiliations

  1. 1.Department of OrthopaedicsZhongshan Hospital of Fudan UniversityShanghaiChina

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